How to increase vasopressin?

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Increasing ADH to Reduce Nighttime Urination Naturally

Many people have problems with urinating too often during the night. It can be very annoying if it persists and can increase stress levels and lead to heightened irritability during the day when it affects sleep quality.

The good news is that most people can eliminate this problem, also known as Nocturia, by increasing the production of ADH (Antidiuretic Hormone) with a proper diet and supplements.

What Is ADH?

Antidiuretic Hormone (ADH) or Vasopressin is a hormone produced in the adjacent hypothalamus in the brain and then stored in the pituitary gland where it is released according to need.

Its primary role is to keep the amount of water in your body balanced and to balance your blood pressure either by constricting blood vessels when the blood pressure is low or increasing the amount of water reabsorbed back into the circulation from the filtrate in the kidneys.

A regular amount of ADH in your body makes sure that you’re well hydrated, which results in a better mood, and better health and wellbeing.

Additionally, ADH also has a role in improving memory , in the release of stress hormones, regulating body temperature, social and sexual behavior, and the circadian rhythm.

ADH production and release is very active during the night reducing the need for urination which is why we rarely need to wake up after a few hours to visit the bathroom. ADH production also supports liver health.

Reasons For Low ADH Levels

Lower levels of ADH is caused by one of two reasons and is known as diabetes insipidus. The reasons for low circulating ADH levels involve either a decrease in the production of ADH by the adjacent hypothalamus or a decreased release of ADH by the pituitary gland. Common symptoms include excessive urination, which is called polyuria, followed by extreme thirst, which is called polydipsia.

With aging, ADH production decreases. When your body is not producing enough ADH, it will excrete too much water, which inevitably results in constant thirst and frequent toilet visits, leading to dehydration.

Low levels are also connected to bed-wetting in children.

How To Increase ADH Levels Naturally

Firstly, plain and simple advice involves drinking less beverages after 4:00 PM, especially avoid alcohol and caffeinated beverage consumption after this time since they are diuretics, leading your body to produce more urine.

When it comes to supplements, Forskolin Root Extract is known to have a significant impact on ADH release. It’s made from the root of a traditional Ayurvedic medicine plant. Besides the many positive effects it has, one of them is causing a higher release of ADH However; you should consult with your doctor before taking this supplement as it shouldn’t be mixed with certain medications including beta-blockers, calcium channel blockers, clonidine and blood pressure lowering drugs.

When it comes to your diet, salt consumption will affect how often you visit the toilet. Decreasing salt intake has been shown to have a positive effect on the frequency of urination, especially at night. Also, when using salt, aim to use natural unrefined salts that are rich in trace minerals, are not exposed to harsh chemicals and do not have plastics in them, for example, Dead Sea Salt and salt from the Colima mines of Mexico, although in low quantities.

Although there are no research studies done on the consumption of raisins before bed to reduce nighttime urination, apparently for some people it really works and has excellent results. Since there is no reason not to consume raisins before bedtime, I do recommend trying.

Additionally, glycine, an amino acid, is linked to an increase in ADH release. To increase the amount of glycine you consume on a plant-based diet, increase your intake of peas, beans of all sorts and legumes. You may also consider taking a glycine supplement, but this is not recommended during pregnancy or lactation, for young children, or people with kidney or liver disease. Otherwise, you may try taking a glycine supplement before bedtime 2 nights a week and see if it helps to reduce your urination wake up frequency.

All in all, a healthier lifestyle with a diet low in salt and rich in legumes supplemented with Forskolin can have a significant impact on your ADH release which will have a substantial effect on your overnight urination.

You and Your Hormones

Alternative names for anti-diuretic hormone

Vasopressin; arginine vasopressin; AVP; ADH

What is anti-diuretic hormone?

Anti-diuretic hormone is made by special nerve cells found in an area at the base of the brain known as the hypothalamus. The nerve cells transport the hormone down their nerve fibres (axons) to the pituitary gland where the hormone is released into the bloodstream. Anti-diuretic hormone helps to control blood pressure by acting on the kidneys and the blood vessels. Its most important role is to conserve the fluid volume of your body by reducing the amount of water passed out in the urine. It does this by allowing water in the urine to be taken back into the body in a specific area of the kidney. Thus, more water returns to the bloodstream, urine concentration rises and water loss is reduced. Higher concentrations of anti-diuretic hormone cause blood vessels to constrict (become narrower) and this increases blood pressure. A deficiency of body fluid (dehydration) can only be finally restored by increasing water intake.

How is anti-diuretic hormone controlled?

The release of anti-diuretic hormone from the pituitary gland into the bloodstream is controlled by a number of factors. A decrease in blood volume or low blood pressure, which occurs during dehydration or a haemorrhage, is detected by sensors (receptors) in the heart and large blood vessels. These stimulate anti-diuretic hormone release. Secretion of anti-diuretic hormone also occurs if the concentration of salts in the bloodstream increases, for example as a result of not drinking enough water on a hot day. This is detected by special nerve cells in the hypothalamus which simulate anti-diuretic hormone release from the pituitary. If the concentration of salts reaches abnormally low levels, this condition is called hyponatraemia. Anti-diuretic hormone is also released by thirst, nausea, vomiting and pain, and acts to keep up the volume of fluid in the bloodstream at times of stress or injury. Alcohol prevents anti-diuretic hormone release, which causes an increase in urine production and dehydration.

What happens if I have too much anti-diuretic hormone?

High levels of anti-diuretic hormone cause the kidneys to retain water in the body. There is a condition called Syndrome of Inappropriate Anti-Diuretic Hormone secretion (SIADH; a type of hyponatraemia) where excess anti-diuretic hormone is released when it is not needed (see the article on hyponatraemia for more information). With this condition, excessive water retention dilutes the blood, giving a characteristically low salt concentration. Excessive levels of anti-diuretic hormone might be caused by drug side-effects and diseases of the lungs, chest wall, hypothalamus or pituitary. Some tumours (particularly lung cancer), can produce anti-diuretic hormone.

What happens if I have too little anti-diuretic hormone?

Low levels of anti-diuretic hormone will cause the kidneys to excrete too much water. Urine volume will increase leading to dehydration and a fall in blood pressure. Low levels of anti-diuretic hormone may indicate damage to the hypothalamus or pituitary gland, or primary polydipsia (compulsive or excessive water drinking). In primary polydipsia, the low level of anti-diuretic hormone represents an effort by the body to get rid of excess water. Diabetes insipidus is a condition where you either make too little anti-diuretic hormone (usually due to a tumour, trauma or inflammation of the pituitary or hypothalamus), or where the kidneys are insensitive to it. Diabetes insipidus is associated with increased thirst and urine production.

Last reviewed: Jan 2015

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Antidiuretic Hormone (ADH) Test

The normal range for ADH is 1-5 picograms per milliliter (pg/mL). Normal ranges can vary slightly among different laboratories. ADH levels that are too low or too high can be caused by a number of different problems.

ADH deficiency

Too little ADH in your blood may be caused by compulsive water drinking or low blood serum osmolality, which is the concentration of particles in your blood.

A rare water metabolism disorder called central diabetes insipidus is sometimes the cause of ADH deficiency. Central diabetes insipidus is marked by a decrease in either the production of ADH by your hypothalamus or the release of ADH from your pituitary gland.

Common symptoms include excessive urination, which is called polyuria, followed by extreme thirst, which is called polydipsia.

People with central diabetes insipidus are often extremely tired because their sleep is frequently interrupted by the need to urinate. Their urine is clear, odorless, and has an abnormally low concentration of particles.

Central diabetes insipidus can lead to severe dehydration if it’s left untreated. Your body won’t have enough water to function.

This disorder is not related to the more common diabetes, which affects the level of the hormone insulin in your blood.

Excess ADH

When there’s too much ADH in your blood, syndrome of inappropriate ADH (SIADH) may be the cause. If the condition is acute, you may have a headache, nausea, or vomiting. In severe cases, coma and convulsions can occur.

Increased ADH is associated with:

  • leukemia
  • lymphoma
  • lung cancer
  • pancreatic cancer
  • bladder cancer
  • brain cancer
  • systemic cancers that produce ADH
  • Guillain-Barré syndrome
  • multiple sclerosis
  • epilepsy
  • acute intermittent porphyria, which is a genetic disorder that affects your production of heme, an important component of blood
  • cystic fibrosis
  • emphysema
  • tuberculosis
  • HIV
  • AIDS

Dehydration, brain trauma, and surgery can also cause excess ADH.

Nephrogenic diabetes insipidus is another very rare disorder that may affect ADH levels. If you have this condition, there’s enough ADH in your blood, but your kidney can’t respond to it, resulting in very dilute urine. The signs and symptoms are similar to central diabetes insipidus. They include excessive urination, which is called polyuria, followed by extreme thirst, which is called polydipsia. Testing for this disorder will likely reveal normal or high ADH levels, which will help distinguish it from central diabetes insipidus.

Nephrogenic diabetes insipidus is not related to the more common diabetes mellitus, which affects the level of insulin hormone in the blood.

What Is Vasopressin?

This natural hormone is used in the management of several life-threatening conditions, including bleeding abnormalities and septic shock.

Vasopressin is a naturally occurring hormone that helps control various bodily functions.

By maintaining the appropriate volume of water in the space that surrounds cells within the body, vasopressin allows proper cellular function.

Vasopressin (also called antidiuretic hormone) plays a role in regulating the circadian rhythm — the periods of sleepiness and wakefulness in a 24-hour cycle.

Vasopressin also helps maintain the body’s internal temperature, its blood volume, and the proper flow of urine from the kidneys.

Both men and women naturally produce vasopressin, yet men experience its effects more strongly because of how it interacts with the male sex hormone testosterone.

Nerve cells at the base of the brain (hypothalamus) make and transport vasopressin to the pituitary gland, which then releases the hormone into the blood stream.

Pain, stress, and certain drugs — such as opiates (narcotics) — can trigger the release of vasopressin.

What Is SIADH?

If your body produces too much vasopressin, your kidneys may retain water.

A condition called syndrome of inappropriate antidiuretic hormone secretion (SIADH) can occur when the body produces too much vasopressin.

In SIADH, excess water retention dilutes the blood, resulting in a low sodium concentration.

Excess vasopressin can be caused by:

  • Drug side effects
  • Diseases of the lungs, chest wall, hypothalamus, or pituitary gland
  • Tumors, especially cancerous ones

What Does Not Enough Vasopressin Do?

If you don’t have enough vasopressin, your kidneys may excrete too much water. This causes frequent urination and can lead to dehydration, as well as low blood pressure.

Lack of vasopressin can be caused by:

  • Damage to the hypothalamus or pituitary gland
  • Drinking an excessive amount of water

Vasopressin in Medical Practice

While vasopressin occurs naturally in the body, healthcare providers also use a synthetic vasopressin drug to help manage the following conditions:

  • Diabetes insipidus (a condition in which the kidneys are insensitive to vasopressin because of a tumor, trauma, medication side effect, or inflammation of the pituitary gland or hypothalamus, leading to water loss through frequent urination)
  • Bleeding abnormalities such as von Willebrand disease and mild hemophilia A
  • Esophageal variceal hemorrhage (in which veins in the esophagus become enlarged and bleed)
  • Asystolic cardiac arrest (in which the heart stops beating, with no electrical activity detected)
  • Septic shock (a serious condition involving extremely low blood pressure caused by an infection)

Vasopressin is given in a hospital or clinical setting, and is administered by injection into a muscle or vein.

If you have diabetes insipidus and don’t need to be treated in a clinical setting, your healthcare provider may show you how to prepare and inject vasopressin at home.

Vasopressin

Generic Name: vasopressin (VAY soe PRES in)
Brand Name: Vasostrict, Pitressin

Medically reviewed by Drugs.com on Mar 11, 2019 – Written by Cerner Multum

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What is vasopressin?

Vasopressin is a man-made form of a hormone called “anti-diuretic hormone” that is normally secreted by the pituitary gland. Vasopressin acts on the kidneys and blood vessels.

Vasopressin helps prevent loss of water from the body by reducing urine output and helping the kidneys reabsorb water into the body. Vasopressin also raises blood pressure by narrowing blood vessels.

Vasopressin is used to treat diabetes insipidus, which is caused by a lack of a naturally occurring pituitary hormone in the body. Vasopressin is also used to treat or prevent certain conditions of the stomach after surgery or during abdominal x-rays.

Vasopressin may also be used for purposes not listed in this medication guide.

Important Information

Follow your doctor’s instructions about the amount of liquids you should drink during your treatment with vasopressin. In some cases, drinking too much liquid can be as unsafe as not drinking enough.

Before taking this medicine

You should not be treated with vasopressin if you are allergic to it.

To make sure vasopressin is safe for you, tell your doctor if you have:

  • coronary artery disease (hardened arteries);

  • congestive heart failure;

  • kidney disease;

  • asthma;

  • migraine headaches; or

  • epilepsy or other seizure disorder.

Tell your doctor if you are pregnant. Vasopressin can cause premature labor contractions if you receive vasopressin during the second or third trimester of pregnancy.

It is not known whether vasopressin passes into breast milk or if it could harm a nursing baby. Tell your doctor if you are breast-feeding a baby.

How is vasopressin given?

Vasopressin is injected into a muscle or under the skin, or into a vein through an IV. A healthcare provider will give you this injection.

Vasopressin is usually given as needed to help control your condition. The time interval between doses will depend on how your body responds to the medication.

To treat diabetes insipidus, vasopressin is sometimes given into the nose by nasal spray or medicine dropper, or insertion of a cotton pad that has been soaked in vasopressin.

When used for abdominal x-ray, vasopressin injections are usually given at 2 hours before and 30 minutes before your x-ray. Your doctor may also recommend you receive an enema before you receive your first dose of vasopressin.

Vasopressin can cause temporary side effects such as nausea, stomach pain, or “blanching” of your skin (pale spots when you press on the skin).

Drinking 1 or 2 glasses of water each time you receive an injection may help ease these side effects. If you are receiving this medicine in your vein through an IV, you may be told not to drink water for a certain period of time.

While using vasopressin, you may need frequent blood tests. Your heart function may also need to be checked using an electrocardiograph or ECG (sometimes called an EKG).

Follow your doctor’s instructions about the amount of liquids you should drink during your treatment with vasopressin. In some cases, drinking too much liquid can be as unsafe as not drinking enough.

What happens if I miss a dose?

Because you will receive vasopressin in a medical setting, you are not likely to miss a dose.

What happens if I overdose?

Since this medication is given by a healthcare professional in a medical setting, an overdose is unlikely to occur.

What should I avoid while receiving vasopressin?

Avoid drinking alcohol during your treatment with vasopressin. Alcohol can make vasopressin less effective.

Vasopressin side effects

Get emergency medical help if you have signs of an allergic reaction: hives; difficult breathing; swelling of your face, lips, tongue, or throat.

Tell your caregivers right away if you have:

  • chest pain or tight feeling;

  • severe or pounding headache, severe drowsiness, feeling very weak;

  • slow heart rate, weak pulse, fainting, slow breathing;

  • loss of color in your lips or around your mouth;

  • numbness or tingling in your hands or feet; or

  • pain or loss of feeling anywhere in your body.

Common side effects may include:

This is not a complete list of side effects and others may occur. Call your doctor for medical advice about side effects. You may report side effects to FDA at 1-800-FDA-1088.

What other drugs will affect vasopressin?

Other drugs may interact with vasopressin, including prescription and over-the-counter medicines, vitamins, and herbal products. Tell each of your health care providers about all medicines you use now and any medicine you start or stop using.

Further information

Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.

Always consult your healthcare provider to ensure the information displayed on this page applies to your personal circumstances.

Copyright 1996-2018 Cerner Multum, Inc. Version: 3.03.

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Vasopressin and its role in critical care

Vasopressin or antidiuretic hormone is a potent endogenous hormone which is responsible for regulating plasma osmolality and volume. It acts as a neurotransmitter in the brain to control circadian rhythm, thermoregulation, and adrenocorticotrophic hormone release (ACTH). The therapeutic use of vasopressin has become increasingly important in the critical care environment in the management of cranial diabetes insipidus, bleeding abnormalities, oesophageal variceal haemorrhage, asystolic cardiac arrest, and septic shock.

Physiology

Vasopressin is a nonapeptide, synthesized as a pro-hormone in magnocellular neurone cell bodies of the paraventricular and supraoptic nuclei of the posterior hypothalamus. It is bound to a carrier protein, neurohypophysin, and transported along the supraoptic hypophyseal tract to the axonal terminals of magnocellular neurones located in the posterior pituitary. Synthesis, transport, and storage takes 1–2 h. Normal plasma concentrations are <4 pg ml−1. It has a half-life of 10–35 min, being metabolized by vasopressinases which are found in the liver and kidney. Vasopressin acts on V1, V2, V3, and oxytocin-type receptors (OTR).

V1 receptors are found on vascular smooth muscle of the systemic, splanchnic, renal, and coronary circulations. They are also located on myometrium and platelets. These G-protein- coupled receptors activate phospholipase C via Gq G-protein, which ultimately leads to an increase in intracellular calcium. The major effect is to induce vasoconstriction, the magnitude of which is dependent on the vascular bed. In the pulmonary circulation, vasodilation is produced via nitric oxide release.

V2 receptors are predominantly located in the distal tubule and collecting ducts of the kidney. These G-protein-coupled receptors stimulate Gs G-protein to activate adenylate cyclase, increasing CAMP, causing the mobilization of aquaporin channels. These channels insert into the apical membrane of the distal tubules and collecting duct cells. V2 receptors are essential for plasma volume and osmolality control. Their presence on endothelial cells induces the release of Von Willebrand Factor (VWF) and Factor VIII:coagulant (FVIII:c). VWF protects FVIII from breakdown in plasma and is important in binding platelets to the site of bleeding.

V3 receptors are found mainly in the pituitary. They are Gq-coupled G-protein receptors which increase intracellular calcium when activated. They are thought to be involved in ACTH release and may act as a neurotransmitter or mediator involved with memory consolidation or retrieval and body temperature regulation.1, 2

Vasopressin has equal affinity for OTR as oxytocin. Activation of these receptors raises intracellular calcium via the phospholipase C and phosphoinositide pathway. They are found predominantly on myometrium and vascular smooth muscle. In addition, they are located on vascular endothelial cells where they increase constitutive endothelial nitric oxide synthase activity, increasing nitric oxide, which is a potent vasodilator. It is postulated that OTR placement on vascular endothelium and their subsequent activation may account for vasopressin’s selective response on different vascular beds. V1 and V2 receptors located on the vascular endothelium may also have a role by increasing NO production.3

Control of release

Table 1 illustrates the factors which affect the release of vasopressin. Most factors (physical or chemical) cause direct stimulation of vasopressin release. Hypoxaemia and acidosis stimulate the carotid body chemoreceptors causing vasopressin release. Catecholamine stimulation of central adrenergic receptors has a variety of effects on vasopressin release. At low concentration, catecholamines activate α1 receptors inducing vasopressin release. At higher concentration, their actions on α2 and β receptors inhibit vasopressin release.3

Table 1

The major factors involved in the release of vasopressin from the posterior pituitary. *Norepinephrine can stimulate release by α1 receptors and inhibit release by stimulation of α2 and β receptors

Stimulate release Inhibit release
Increasing plasma osmolality Decreasing plasma osmolality
Reduced plasma volume Increased plasma volume
Chemical mediators Chemical mediators
 Norepinephrine*, dopamine, acetylcholine, histamine, prostaglandins, angiotensin II, endotoxin, cytokines  Opioids, GABA, ANP, norepinephrine*
Nausea, vomiting
Pain, Stress
Hypoxia, Paco2, acidosis
Exercise, IPPV
Stimulate release Inhibit release
Increasing plasma osmolality Decreasing plasma osmolality
Reduced plasma volume Increased plasma volume
Chemical mediators Chemical mediators
 Norepinephrine*, dopamine, acetylcholine, histamine, prostaglandins, angiotensin II, endotoxin, cytokines  Opioids, GABA, ANP, norepinephrine*
Nausea, vomiting
Pain, Stress
Hypoxia, Paco2, acidosis
Exercise, IPPV

Table 1

The major factors involved in the release of vasopressin from the posterior pituitary. *Norepinephrine can stimulate release by α1 receptors and inhibit release by stimulation of α2 and β receptors

Stimulate release Inhibit release
Increasing plasma osmolality Decreasing plasma osmolality
Reduced plasma volume Increased plasma volume
Chemical mediators Chemical mediators
 Norepinephrine*, dopamine, acetylcholine, histamine, prostaglandins, angiotensin II, endotoxin, cytokines  Opioids, GABA, ANP, norepinephrine*
Nausea, vomiting
Pain, Stress
Hypoxia, Paco2, acidosis
Exercise, IPPV
Stimulate release Inhibit release
Increasing plasma osmolality Decreasing plasma osmolality
Reduced plasma volume Increased plasma volume
Chemical mediators Chemical mediators
 Norepinephrine*, dopamine, acetylcholine, histamine, prostaglandins, angiotensin II, endotoxin, cytokines  Opioids, GABA, ANP, norepinephrine*
Nausea, vomiting
Pain, Stress
Hypoxia, Paco2, acidosis
Exercise, IPPV

The most potent stimulus for vasopressin release is an increased plasma osmolality. Central osmoreceptors in the subfornical organ nuclei, located outside the blood–brain barrier, monitor systemic plasma osmolality. Peripheral osmoreceptors are found in the portal veins and give early warning of ingested food and fluid osmolality. Signals are transmitted via the vagus to the nucleus tractus solitarius, area postrema, and ventrolateral medulla, and finally to the paraventricular nuclei and supraoptic nuclei, where vasopressin is manufactured in the magnocellular neurone cell bodies. Osmolality is finely controlled in the range of 275–290 mOsm kg−1. A 2% decrease in total body water results in a doubling of the vasopressin plasma concentration. This acts on V2 receptors increasing the collecting duct permeability to water. Conversely, a 2% increase in total body water will result in maximal suppression of vasopressin release and maximally dilute urine of 100 mOsm kg−1.

Plasma volume and the resultant change in arterial pressure are less sensitive controllers of vasopressin release, but the potential response far exceeds that induced by changes in plasma osmolality. A 20–30% reduction in mean arterial pressure (MAP) is needed to induce a response. This results in a reduced arterial baroreceptor output causing an exponential increase in vasopressin release. The response to a reduction in plasma volume and its effect on vasopressin release is not well defined but is probably qualitatively and quantitatively similar. An 8–10% reduction in plasma volume, detected by atrial stretch receptors, is required to induce an exponential increase in vasopressin release. A reduction in plasma volume increases the sensitivity of the osmoreceptors and vice versa. However, as the plasma volume decreases, it becomes increasingly difficult to maintain a normal plasma osmolality. The defence of plasma volume always takes precedence over plasma osmolality. Less is known about acute elevations in arterial pressure and volume, but both appear to suppress vasopressin release.4

Pharmacology

In most mammals, 8-arginine vasopressin is the native antidiuretic hormone. Original preparations were extracted from posterior pituitary cells (Fig. 1). It is now made as a synthetic peptide, argipressin. It is metabolized in a way similar to endogenous vasopressin and has a half-life of 24 min.

Fig. 1

The structure of vasopressin (8-arginine-vasopressin) which is the exact synthetic protein of human endogenous vasopressin is shown. Terlipressin (triglycyl-lysine-vasopressin) is a prodrug requiring the enzymic cleavage of the three glycyl residues to form the active lysine vasopressin found naturally in pigs. Desmopressin, DDAVP, is an arginine vasopressin analogue.

Fig. 1

The structure of vasopressin (8-arginine-vasopressin) which is the exact synthetic protein of human endogenous vasopressin is shown. Terlipressin (triglycyl-lysine-vasopressin) is a prodrug requiring the enzymic cleavage of the three glycyl residues to form the active lysine vasopressin found naturally in pigs. Desmopressin, DDAVP, is an arginine vasopressin analogue.

Tri-glycyl-lysine-vasopressin is terlipressin or glypressin. Arginine is replaced with lysine at position 8 and has three glycine residues at the beginning of the peptide. The lysine substitution makes it identical to pig vasopressin. The three glycine residues make terlipressin a prodrug. In the body, these are enzymatically cleaved by endothelial peptidases to produce lysine vasopressin. It has an elimination half-life of 50 min, but an effect half-life of 6 h.

Desmopressin (1-deamino-8-O-arginine-vasopressin, DDAVP) is a synthetic analogue of arginine vasopressin. It has 10 times the antidiuretic action of vasopressin, but 1500 times less vasoconstrictor action. These modifications make metabolism slower (half-life of 158 min).

Therapeutic uses

Cranial diabetes insipidus

The causes of diabetes insipidus are listed in Table 2. In cranial diabetes insipidus, there is a lack of vasopressin due to destruction of part or all of the hypothalamus or pituitary gland. This is in contrast to nephrogenic diabetes insipidus where there is a resistance of the kidney to vasopressin’s action. Clinically, the patient produces vast quantities of dilute urine. The key feature is that urine osmolality is inappropriately low compared with the plasma osmolality. Desmopressin (DDAVP) can reduce the polyuria, nocturia, and polydypsia. It is given nasally, sublingually, i.m., or if in critical care setting, i.v..

Table 2

The causes of diabetes insipidus

Cranial Nephrogenic
Familial Familial
Idiopathic Idiopathic
 Neurosurgery
Tumours
 Craniopharyngioma; hypothalamic gliomas; metastases, e.g. breast; lymphoma/leukaemia Renal tubular acidosis; hypokalaemia; hypercalcaemia
Infections Drugs
 Tuberculosis; meningitis; cerebral abscess  Lithuim; glibenclamide; demeclocycline
Infiltrations
 Sarcoidosis
Vascular
 Haemorrhage; aneurysms; thrombosis
Trauma
 Head injury
Cranial Nephrogenic
Familial Familial
Idiopathic Idiopathic
 Neurosurgery
Tumours
 Craniopharyngioma; hypothalamic gliomas; metastases, e.g. breast; lymphoma/leukaemia Renal tubular acidosis; hypokalaemia; hypercalcaemia
Infections Drugs
 Tuberculosis; meningitis; cerebral abscess  Lithuim; glibenclamide; demeclocycline
Infiltrations
 Sarcoidosis
Vascular
 Haemorrhage; aneurysms; thrombosis
Trauma
 Head injury

Table 2

The causes of diabetes insipidus

Cranial Nephrogenic
Familial Familial
Idiopathic Idiopathic
 Neurosurgery
Tumours
 Craniopharyngioma; hypothalamic gliomas; metastases, e.g. breast; lymphoma/leukaemia Renal tubular acidosis; hypokalaemia; hypercalcaemia
Infections Drugs
 Tuberculosis; meningitis; cerebral abscess  Lithuim; glibenclamide; demeclocycline
Infiltrations
 Sarcoidosis
Vascular
 Haemorrhage; aneurysms; thrombosis
Trauma
 Head injury
Cranial Nephrogenic
Familial Familial
Idiopathic Idiopathic
 Neurosurgery
Tumours
 Craniopharyngioma; hypothalamic gliomas; metastases, e.g. breast; lymphoma/leukaemia Renal tubular acidosis; hypokalaemia; hypercalcaemia
Infections Drugs
 Tuberculosis; meningitis; cerebral abscess  Lithuim; glibenclamide; demeclocycline
Infiltrations
 Sarcoidosis
Vascular
 Haemorrhage; aneurysms; thrombosis
Trauma
 Head injury

Syndrome of inappropriate antidiuretic hormone

The syndrome of inappropriate antidiuretic hormone is a form of hyponatraemia where the level of antidiuretic hormone is inappropriate to the osmotic or volume stimuli, almost a reverse of cranial diabetes insipidus. The causes can be grouped into ectopic secretion by tumours, particularly small cell carcinoma of the lung, central nervous system disorders, including tumours, infection, and trauma, and pulmonary lesions, mainly infections and drugs, for example, carbamazepine. There are strict diagnostic criteria which include the need for normovolaemia, normal endocrine, cardiac, and liver function, in the presence of urinary osmolality greater than plasma osmolality. Treatment is the correction of hyponatraemia appropriate to the speed of onset and eradication of the underlying cause.

Bleeding abnormalities

Vasopressin acts via extra-renal V2 receptors to increase predominantly FVIII:c and VWF. These actions are very useful in certain types of Von Willebrand disease and in mild forms of haemophilia A, where there is a relative deficiency of FVIII:c. Likewise, in patients with impaired platelet function due to drugs such as aspirin or renal failure, DDAVP (0.3 µg kg−1 i.v. over 15–30 min) may be useful before minor surgical procedures. The exact mechanism of its effect in these situations is not fully understood, but the increase in FVIII levels which allows activation of FX and the more efficient activation of platelets are all important.5

Oesophageal variceal haemorrhage

In chronic liver disease, fibrosis of the liver results in an increase in portal venous pressure as the mesenteric blood requires increasing pressure to flow through the scarred liver. Eventually, collateral circulation opens up to allow the return of blood to the systemic circulation through shunts. One of these is the intrinsic and extrinsic gastro-oesophageal veins. These veins become increasing dilated, forming varices. Vasopressin, acting via V1 receptors, reduces portal blood flow, portal systemic collateral blood flow, and variceal pressure. Its side-effects include increased peripheral vascular resistance, reduced cardiac output, and decreased coronary blood flow. The combined use of glyceryl trinitrate with vasopressin has been shown to reduce these side-effects. Terlipressin, a prodrug of vasopressin, is more commonly used. A Cochrane review6 found that terlipressin produced a relative risk reduction in mortality from variceal haemorrhage of 34% compared with placebo. The i.v. dose is typically 2 mg 4 hourly.

Asystolic cardiac arrest

Epinephrine has been considered the main drug for resuscitation for over 100 years. Recently, some doubt has been cast over its use. Patients who were sucessfully resuscitated with epinephrine showed increased myocardial oxygen consumption and ventricular arrhythmias, ventilation–perfusion mismatch, and myocardial dysfunction post-resuscitation. In survivors of cardiac arrest, vasopressin levels have been shown to be higher than in those who died. Wenzel and colleagues7 performed a multicentre randomized double-blinded trial in 1186 patients who had an out-of-hospital cardiac arrest. They were randomly assigned to receive either 40 IU of vasopressin or 1 mg of epinephrine during resuscitation. In the asystolic group, significantly more patients reached hospital who received vasopressin, compared with those who received epinephrine (29% vs 20%, P=0.02). In the vasopressin group, 4.7% were discharged from hospital compared with 1.5% in the epinephrine group. Of the 732 patients where spontaneous circulation was not achieved initially, in those who received vasopressin then epinephrine, 25.6% reached hospital and 6.7% were discharged compared with 16.4% and 1.7% of those who received epinephrine alone. There was no difference between the groups in those patients who suffered pulseless electrical activity or ventricular fibrillation cardiac arrests. There is a suggestion that vasopressin may work better than epinephrine in hypoxaemic, acidotic conditions. Other trials have shown a varying response to vasopressin in all forms of cardiac arrest. These differences may be related to poor initial cardiopulmonary resuscitation and prolonged time to advanced life support. The trend suggests a better outcome in the vasopressin groups, if there was delayed or prolonged resuscitation. The use of epinephrine in resuscitation is universal, yet there is a paucity of evidence to show it improves survival in humans. The European resuscitation guidelines state there is insufficient evidence for the use of vasopressin with or instead of epinephrine in any type of cardiac arrest and that further evidence is required.

Septic shock

The cause of hypotension in septic shock is multifactorial. Inappropriate vasodilation compromises organ perfusion. Fluid, vasoconstrictors, and inotropes are usually used to maintain arterial pressure. Norepinephrine is the most commonly used vasoconstrictor. Unfortunately, cardiac and vascular smooth muscle can become resistant, requiring increasing doses of norepinephrine. This produces adverse effects which include increasing tissue oxygen demand, reducing renal and mesenteric blood flow, pulmonary hypertension, and arrhythmias. Vasopressin’s role in maintaining arterial pressure has been investigated in septic shock. Landry and colleagues8 were the first to show vasopressin was inappropriately low in vasodilatory septic shock. In 19 patients with vasodilatory septic shock, vasopressin levels were 3.1 pg ml−1 with systolic arterial pressure (SAP) of 92 mm Hg and cardiac output of 8 litre min−1 (all data are given as mean values). In patients who had cardiogenic shock, vasopressin levels were 22.7 pg ml−1. If an infusion of 0.04 IU min−1 of vasopressin was started, SAP increased from 92 to 146 mm Hg and then decreased when vasopressin was withdrawn. An infusion of 0.01 IU min−1 was shown to increase vasopressin levels into the normal range in these patients suggesting that reduced secretion, not increased metabolism, was the cause of vasopressin deficiency.

Why vasopressin is low in septic shock is open to conjecture. There appears to be a biphasic response. Initially, vasopressin levels are elevated but 6 h after the onset of hypotension levels may be inappropriately low for the degree of hypotension. Possible explanations include exhaustion of stores and autonomic nervous system dysfunction. Large doses of norepinephrine are inhibitory to vasopressin release. Nitric oxide, an inflammatory mediator, may also act on the pituitary to prevent release.4

Numerous case studies and small trials show vasopressin increases arterial pressure in septic shock. The largest randomized prospective controlled study was published in 2003 by Dunser and colleagues.9 In this study, 48 patients with catecholamine-resistant vasodilatory shock were prospectively randomized to receive a combined infusion of vasopressin, 4 IU h−1 (0.066 IU min−1) and norepinephrine or norepinephrine alone to maintain a MAP above 70 mm Hg. The vasopressin group showed a significant increase in MAP, cardiac index, systemic vascular resistance index, and left-ventricular stroke work index as well as reduced norepinephrine requirements and heart rates. Compared with the norepinephrine group, there was better preservation of gut mucosal blood flow and a significantly lower incidence of tachyarrhythmias.

In sepsis, there is an increased sensitivity to vasopressin. The theories suggested include increased receptor density as endogenous vasopressin levels are reduced and alteration in receptor expression on different vascular beds with possible changes in signal transduction. Vasopressin and norepinephrine are believed to have a synergistic action when used together. Vasopressin increases intracellular calcium, maintaining vascular tone when norepinephrine receptor sensitivity is reduced. In endotoxic shock, excessive activation of potassium-sensitive ATP channels causes increased potassium conductance leading to the closure of voltage-gated calcium channels and the reduction in vascular tone. Vasopressin blocks these potassium-sensitive ATP channels, restoring vascular tone. The additional action on other hormone systems like cortisol and endothelin1 may also play a role in the maintenance of arterial pressure.

The use of vasopressin is not without side-effects. Myocardial ischaemia may occur, but this effect is limited by avoiding high doses. A varied effect on splanchnic blood flow has been found. At lower doses, a minimal response occurs provided the patients are adequately intravascularly filled. Both the dosage and timing of the use of vasopressin in sepsis are currently under investigation. However, in the literature, a dose range of 0.01–0.04 IU min−1 is commonly used to replace falling vasopressin levels. It is usually started when increasing norepinephrine doses are being used to maintain arterial pressure. It is best administered through central access as extravasations can cause skin necrosis.

The vasopressin and septic shock trial (VASST)10 was the first multicentre, blinded randomized trial comparing low dose vasopressin with norepinephrine in 778 patients with septic shock. The use of vasopressin did not reduce mortality but was shown to be as safe as norepinephrine. Vasopressin is acknowledged as an adjunct vasopressor in the Surviving Sepsis Guidelines and certainly its use is increasing, but further investigations are needed to define its exact role in sepsis related hypotension.

1 Holmes CL , Patel BM , Russell JA , Walley KR . The physiology of vasopresin relevant to the management of septic shock, Chest, 2001, vol. 120 (pg. 989-1002) 2 Kam PCA , Williams S , Yoong FFY . Vasopressin and terlipressin: pharmacology and its clinical relevance, Anaesthesia, 2004, vol. 59 (pg. 993-1001) 3 Barrett LK , Singer M , Clapp LH . Vasopressin: mechanism of action on vasculature in health and in septic shock, Crit Care Med, 2007, vol. 35 (pg. 33-40) 4 Mutlu GM , Factor P . Role of vasopressin in the management of septic shock, Intensive Care Med, 2004, vol. 30 (pg. 1276-91) 5 Ozgonenel B , Rajpurkar M , Lusher JM . How do you treat bleeding disorders with desmopressin, Postgrad Med J, 2007, vol. 83 (pg. 159-63) 6 Ioannou G , Doust J , Rockey DC . Terlipressin in acute oesophageal variceal haemorrhage, Cochrane Database Syst Rev, 2003 CD002147. doi:10.1002/14651858.CD002147 7 Wenzel V , Krismer AC , Arntz R , Sitter H , Stadlbauer KH , Linner KH . A comparison of vasopressin and epinephrine for out of hospital cardiopulmonary resuscitation, N Engl J Med, 2004, vol. 350 (pg. 105-13) 8 Landry DW , Levin HR , Gallant EM, , et al. Vasopressin deficiency contributes to the vasodilation of septic shock, Circulation, 1997, vol. 95 (pg. 1122-5) 9 Dunser MW , Mayr AJ , Ulmer H, , et al. Arginine vasopressin in advanced vasodilatory shock: a prospective randomised control study, Circulation, 2003, vol. 107 (pg. 2313-9) 10 Russell JA , Walley KR , Singer J , Gordon AC , Hebert PC , Cooper J . Vasopressin versus norepinephrine infusion in patients with septic shock, N Engl J Med, 2008, vol. 358 (pg. 877-87) © The Board of Management and Trustees of the British Journal of Anaesthesia . All rights reserved. For Permissions, please email: [email protected]

What is arginine vasopressin (AVP) hormone and how does it work?

Author

Christie P Thomas, MBBS, FRCP, FASN, FAHA Professor, Department of Internal Medicine, Division of Nephrology, Departments of Pediatrics and Obstetrics and Gynecology, Medical Director, Kidney and Kidney/Pancreas Transplant Program, University of Iowa Hospitals and Clinics
Christie P Thomas, MBBS, FRCP, FASN, FAHA is a member of the following medical societies: American College of Physicians, American Heart Association, American Society of Nephrology, Royal College of Physicians
Disclosure: Nothing to disclose.

Specialty Editor Board

Eleanor Lederer, MD, FASN Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital
Eleanor Lederer, MD, FASN is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, Phi Beta Kappa
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Society of Nephrology<br/>Received income in an amount equal to or greater than $250 from: Healthcare Quality Strategies, Inc<br/>Received grant/research funds from Dept of Veterans Affairs for research; Received salary from American Society of Nephrology for asn council position; Received salary from University of Louisville for employment; Received salary from University of Louisville Physicians for employment; Received contract payment from American Physician Institute for Advanced Professional Studies, LLC for independent contractor; Received contract payment from Healthcare Quality Strategies, Inc for independent cont.

Chief Editor

Vecihi Batuman, MD, FASN Huberwald Professor of Medicine, Section of Nephrology-Hypertension, Tulane University School of Medicine; Chief, Renal Section, Southeast Louisiana Veterans Health Care System
Vecihi Batuman, MD, FASN is a member of the following medical societies: American College of Physicians, American Society of Hypertension, American Society of Nephrology, International Society of Nephrology, Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

Additional Contributors

Mony Fraer, MD, MHCDS, FACP, FASN Associate Professor, Division of Nephrology, Department of Medicine, University of Iowa Hospitals and Clinics; Staff Physician, Iowa City Veterans Affairs Medical Center
Disclosure: Nothing to disclose.

Acknowledgements

Howard A Bessen, MD Professor of Medicine, Department of Emergency Medicine, UCLA School of Medicine; Program Director, Harbor-UCLA Medical Center

Howard A Bessen, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Keenan Bora, MD Fellow, Medical Toxicology, Detroit Medical Center; Attending Physician, Medical Center Emergency Services, Detroit

Keenan Bora, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and American Medical Association

Disclosure: Nothing to disclose.

Meher Chaudhry, MD Chief Resident, Department of Emergency Medicine, Detroit Receiving Hospital, University Health Center

Disclosure: Nothing to disclose.

Sonali Deshmukh, MBBS Consulting Staff, Omaha Nephrology, Nebraska

Sonali Deshmukh, MBBS is a member of the following medical societies: American Society of Nephrology

Disclosure: Nothing to disclose.

R obert J Ferry Jr, MD Chief, Division of Pediatric Endocrinology and Metabolism, Le Bonheur Children’s Hospital; Professor, Department of Pediatrics, University of Tennessee Health Science Center at Memphis; St. Jude Children’s Research Hospital, Memphis, TN; Brigade Surgeon, 36th Sustainment Brigade, U.S. Army; Adjunct Professor, Pediatric Surgery Department, King Saud University, Riyadh, Saudi Arabia

Robert J Ferry Jr, MD is a member of the following medical societies: American Academy of Pediatrics, American Diabetes Association, American Medical Association, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, Society for Pediatric Research, and Texas Pediatric Society

Disclosure: Nutropin Speakers Bureau Honoraria Speaking and teaching; Genotropin Speakers Bureau Honoraria Speaking and teaching; Eli Lilly & Co. Grant/research funds Investigator; MacroGenics, Inc. Grant/research funds Investigator; Ipsen, S.A. (formerly Tercica, Inc.) Grant/research funds Investigator; NovoNordisk SA Grant/research funds Investigator; Diamyd Investigator

Stephen Kemp, MD, PhD Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas College of Medicine and Arkansas Children’s Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, and Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Eleanor Lederer, MD Professor of Medicine, Chief, Nephrology Division, Director, Nephrology Training Program, Director, Metabolic Stone Clinic, Kidney Disease Program, University of Louisville School of Medicine; Consulting Staff, Louisville Veterans Affairs Hospital

Eleanor Lederer, MD is a member of the following medical societies: American Association for the Advancement of Science, American Federation for Medical Research, American Society for Biochemistry and Molecular Biology, American Society for Bone and Mineral Research, American Society of Nephrology, American Society of Transplantation, International Society of Nephrology, Kentucky Medical Association, National Kidney Foundation, and Phi Beta Kappa

Disclosure: Dept of Veterans Affairs Grant/research funds Research

Lynne Lipton Levitsky, MD Chief, Pediatric Endocrine Unit, Massachusetts General Hospital; Associate Professor of Pediatrics, Harvard Medical School

Lynne Lipton Levitsky, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Pediatrics, American Diabetes Association, American Pediatric Society, Endocrine Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Pfizer Grant/research funds P.I.; Tercica Grant/research funds Other; Eli Lily Grant/research funds PI; NovoNordisk Grant/research funds PI

Chike Magnus Nzerue, MD Associate Dean for Clinical Affairs, Vice-Chairman of Internal Medicine, Meharry Medical College

Chike Magnus Nzerue, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Physicians, American College of Physicians-American Society of Internal Medicine, American Society of Nephrology, and National Kidney Foundation

Disclosure: Nothing to disclose.

Jose F Pascual-y-Baralt, MD Chief, Division of Pediatric Nephrology, San Antonio Military Pediatric Center; Clinical Professor, Department of Pediatrics, University of Texas Health Science Campus

Jose F Pascual-y-Baralt, MD is a member of the following medical societies: American Academy of Pediatrics, American Society of Nephrology, American Society of Pediatric Nephrology, Association of Military Surgeons of the US, and International Society of Nephrology

Disclosure: Nothing to disclose.

Alexandr Rafailov, MD Staff Physician, Department of Emergency Medicine, State University of New York Downstate/Kings County Hospital

Disclosure: Nothing to disclose.

Arlan L Rosenbloom, MD Adjunct Distinguished Service Professor Emeritus of Pediatrics, University of Florida; Fellow of the American Academy of Pediatrics; Fellow of the American College of Epidemiology

Arlan L Rosenbloom, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Epidemiology, American Pediatric Society, Endocrine Society, Florida Pediatric Society, Lawson-Wilkins Pediatric Endocrine Society, and Society for Pediatric Research

Disclosure: Nothing to disclose.

Erik D Schraga, MD Consulting Staff, Department of Emergency Medicine, Mills-Peninsula Emergency Medical Associates; Consulting Staff, Permanente Medical Group, Kaiser Permanente, Santa Clara Medical Center

Disclosure: Nothing to disclose.

Richard H Sinert, DO Associate Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Pharmacy Editor, Medscape

Disclosure: Nothing to disclose.

Vasopressin, otherwise known as Antidiuretic Hormone (ADH), has roles in water balance and blood pressure, but it’s also sought after as a smart drug. This post reveals the roles of vasopressin, health implications of high/low levels, and factors that impact secretion.

What is Vasopressin?

Role in the Body

Why is it so important? Vasopressin plays a major role in keeping the body hydrated, the mind sharp, and the mood bright.

  • For athletes: too high vasopressin levels may result in difficulty holding onto salt, a key electrolyte.
  • For those concerned about mental sharpness: vasopressin is considered a “smart drug” by many and is being studied as a treatment for dementia.
  • For those struggling with frequent urination or bedwetting: low vasopressin may play a role.
  • For those who feel nauseated after drinking a lot of water or get headaches after intense exercise: high vasopressin may be involved.
  • For those feeling constantly thirsty and always running to the bathroom, low vasopressin may play a role .
  • It may also play a role in stress and/or chronic inflammation .

Although it’s seldom discussed, even in health circles, vasopressin clearly plays a major role in our everyday health and well-being. This post discusses how it can manifest in different health conditions.

Overview

Vasopressin is otherwise known as Arginine-Vasopressin (AVP) because in most species it contains arginine. It is produced by the hypothalamus and released by the pituitary gland in the brain.

It’s also called Antidiuretic Hormone (ADH) because it reduces urination (diuresis).

Vasopressin is especially active at night, eliminating the need to go to the bathroom every couple of hours, and allowing you to sleep straight through until morning .

Besides helping the body to retain water, is also constricts blood vessels, which increases blood pressure. You can think of it as inhibiting flow – of water and of blood. That’s where the name “vasopressin” comes from – causing a restriction in blood vessels.

How Vasopressin Affects the Brain

It all starts in the brain.

When the brain gets the signal that the body is getting dehydrated (blood pressure is low, blood is highly concentrated), vasopressin is released and the kidneys are given the message to conserve water and prevent the loss of water in the urine. Instead, the urine is more concentrated and water is reabsorbed into the body, diluting the blood, and restoring balance to the body.

Vasopressin does much more than just regulate our water and salt concentrations. It also has a role in memory, regulating blood pressure and body temperature, CRH release, socio-sexual behavior, and even our circadian rhythm .

It can act as a neurotransmitter, and it can stimulate the production of other needed neurotransmitters .

Vasopressin is also considered to be a stress hormone like cortisol or CRH .

Health Effects of Vasopressin

Keep in mind that health effects of vasopressin as a hormone in the body may not translate to the effects of vasopressin administration.

Nootropic Effects

The effects described below are not researched well enough. They stem from low-quality clinical or animal trials.

  • Vasopressin is used as a nootropic/smart drug by some people. It can influence mental clarity, attention to detail, short-term memory and long-term memory .
  • It enhances learning in mice .
  • It is also being studied for the treatment of memory problems associated with aging, dementia, drug toxicity, and amnesia .
  • High Vasopressin can make you more cooperative .

Low Vasopressin

Vasopressin levels are a marker of urine and blood flow. Low or high levels don’t necessarily indicate a problem if there are no symptoms or if your doctor tells you not to worry about it.

The following conditions have been linked with low vasopressin:

Factors That May Increase Vasopressin (AVP Promoters)

Addressing your vasopressin levels won’t necessarily cause improvement in blood and urine flow. The following is a list of factors that impact water balance and that may also increase low vasopressin. Though studies suggest various dietary and lifestyle factors may increase vasopressin, additional large-scale clinical trials are needed.

  • Restricting water
  • Dietary Sodium
  • Standing
  • Exercise
  • Sauna
  • Forskolin/cAMP
  • Glycine
  • Rhodiola – Lowers endopeptidase activity, leading to higher vasopressin. Rhodiola sacra and Rhodiola sachalinensis .
  • Ginkgo – Lowers endopeptidase activity, leading to higher vasopressin
  • Baicalein – Inhibits endopeptidase, raising vasopressin
  • Berberine – Inhibits endopeptidase, raising vasopressin
  • Acetylcholine – Increases vasopressin (in rat studies)
  • Increased IL-1beta
  • Increased Interleukin-6
  • Increased CRH
  • Inhibited IGF-1
  • Increased BMAL1, which is needed for the production of vasopressin
  • Stimulated 5-HT2C receptors, which leads to an increase in vasopressin . Some 5-HT2C activators include Serotonin , Ginseng , and Bacopa (rats) .
  • Nicotine (rabbits, cats, men) .
  • Racetams – Raise Acetylcholine, raising vasopressin
  • Pramiracetam – Inhibits endopeptidase, raising vasopressin .
  • Desmopressin – Synthetic vasopressin that has 10 times the antidiuretic effects of vasopressin, but 1500 times less of the constricting effect on blood vessels .
  • Other Drugs that increase vasopressin: morphine, amitriptyline, barbiturates, desipramine, and carbamazepine (45).

High Vasopressin

Vasopressin levels are a marker of urine and blood flow. Low or high levels don’t necessarily indicate a problem if there are no symptoms or if your doctor tells you not to worry about it.

Associated Conditions

  • Stress – in humans and in rats and mice
  • Pain – in humans
  • High blood pressure
  • Major depression
  • Diabetes (Type 2)
  • Low Cortisol
  • Low sodium/Hyponatremia/Syndrome of Inappropriate Diuretic Hormone (SIADH) secretion
    • Unsteady gait
    • impaired memory
  • Low Thyroid
  • Post Viral Fatigue Syndrome
  • Kidney Stones – Vasopressin causes our urine to be less dilute.
  • High Blood Sugar – Insulin can cause the release of vasopressin . Vasopressin causes insulin release in mice .
  • Low BUN (Blood Urea Nitrogen) levels
  • Low Uric Acid levels particularly in SIADH
  • High CRH – Vasopressin releases CRH
  • Anorexia – vasopressin suppresses appetite

Factors That May Lower Vasopressin (AVP Inhibitors)

Addressing your vasopressin levels won’t necessarily cause improvement in blood and urine flow. The following is a list of factors that impact water balance and that may also reduce high vasopressin. Though studies suggest various dietary and lifestyle factors may increase vasopressin, additional large-scale clinical trials are needed.

Hormones:

  • Increased Progesterone – Progesterone therapy caused a decrease in blood levels of vasopressin .
  • Combined Estrogen with Progesterone – There was no change in blood levels of vasopressin with estrogen treatment alone, but following a combined administration of estrogen and progesterone .
  • Increased Testosterone .

Other:

The Top 10 Ways to Boost Good Feelings

The “love molecule,” oxytocin, is the chemical foundation for trusting others. Activated by positive social interactions, it makes us care about others in tangible ways, and it motivates us to work together for a common purpose.

After a dozen years studying the role oxytocin plays in human behavior, I thought I’d share an answer to the question I am most often asked: How can I raise my levels? Below is my top 10 list.

But first, a short neuroscience digression: The effect of oxytocin, like other signaling chemicals in the brain, is more dependent on changes than on absolute levels. Oxytocin helps us respond appropriately to our social environment by changing its amounts in the brain second by second. Rather than focus on oxytocin levels that are near zero, for most people without a positive social interaction, the better question is how can one increase their level of oxytocin when interacting with others and thereby increase empathy and compassion towards them.

Another neuroscience digression: Because oxytocin is so ancient (a precursor can be traced back at least 400 million years to fish), natural selection has found ways to utilize it in both the brain and the body. Unlike almost every other neurochemical we make, animal studies have shown that the change in oxytocin after a social interaction as measured in the blood reflects changes in oxytocin in the brain. Thus, if an activity causes a spike in oxytocin as measured in the blood, a corresponding spike is likely occurring in the brain. It is brain oxytocin that is most responsible for effects on behavior, and blood oxytocin gives us a window into what occurs in the brain.

The ways to raise oxytocin listed below are based on measuring changes in oxytocin in blood in humans. Many are from my lab and some come from other sources. Variations in protocols and the moderate sample sizes for human studies inhibit comparing the reported average changes in oxytocin across published works. Instead, I’m simply listing the ways to raise oxytocin in order of my personal favorites.

10. Listen with your eyes. Instead of being glued to an electronic device, give the person with you your complete attention. Watch their face and listen to what he or she is telling you.

9. Give a gift. Our first human oxytocin studies showed that receiving gifts raised oxytocin. Why not make this a regular practice? The key is not to expect a gift in return, just surprise someone for no reason.

8. Share a meal. Eating moderately is calming and helps us bond with others. Including a glass of wine is fine, too. You can increase the effect by following #9 and making the meal you share a gift.

7. Meditate while focusing on others. My lab has found that a form of meditation called “metta,” in which one focuses on loving others, is better at fostering social connections than standard mindfulness meditation.

6. Soak in a hot tub. I love to do this with my kids. The warm temperature and time together offer the ability to connect with them. And we all look goofy when we’re wet, making the time even more fun.

5. Use social media. OK, you are doing this anyway, but you should know that 100% of the people I tested using social media had an increase in oxytocin. Just don’t forget to see your Facebook friends in person, too.

4. Ride a roller coaster or jump out of an airplane. Many activities that are moderately stressful and done with one or more other people raise oxytocin. My recent tandem skydive produced a greater than 200% oxytocin spike. Try being a single rider on a roller coaster and you’ll experience an immediate bond with the person next to you.

3. Pet a dog. This doesn’t always work unless the dog belongs to you, but if you identify as a “dog person,” any old dog will raise your oxytocin. The dog won’t complain, either. And once your oxytocin is up, you’ll connect better to the humans around you, too.

2. Use the “L” word. Tell those around you that you love them. Oxytocin is the love molecule so it is part of our evolved biology to love others (both “philia” and “eros”). You’ve got to put it out there to get it back. With friends, too, and maybe even at work.

1. Eight hugs a day. We have shown that touch not only raises oxytocin, but it reduces cardiovascular stress and can improve the immune system, too. Try telling people that you hug rather than shake hands and see what happens when you give others the gift of oxytocin.

Studies show that the more one releases oxytocin, the easier it becomes to do so. That has certainly been my experience in practicing these oxytocin-releasing activities. If you can do all 10, you’ll be an oxytocin master.

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