Clonidine 1 mg



Generic Name: clonidine (oral) (KLOE ni deen)
Brand Names: Catapres, Kapvay

Medically reviewed by Sanjai Sinha, MD Last updated on Dec 4, 2018.

  • Overview
  • Side Effects
  • Dosage
  • Professional
  • Tips
  • Interactions
  • More

What is clonidine?

Clonidine lowers blood pressure by decreasing the levels of certain chemicals in your blood. This allows your blood vessels to relax and your heart to beat more slowly and easily.

The Catapres brand of clonidine is used to treat hypertension (high blood pressure). The Kapvay brand is used to treat attention deficit hyperactivity disorder (ADHD).

Clonidine is sometimes given with other medications.

Important information

Before you take clonidine, tell your doctor if you have heart disease or severe coronary artery disease, a heart rhythm disorder, slow heartbeats, low blood pressure, a history of heart attack or stroke, kidney disease, or if you have ever had an allergic reaction to a Catapres TTS transdermal skin patch.

Before taking this medicine

You should not take this medicine if you are allergic to clonidine.

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

  • heart disease or severe coronary artery disease;

  • heart rhythm disorder, slow heartbeats;

  • low blood pressure, or a history of fainting spells;

  • a history of heart attack or stroke;

  • pheochromocytoma (tumor of the adrenal gland);

  • kidney disease; or

  • if you have ever had an allergic reaction to a Catapres TTS skin patch.

Older adults may be more sensitive to the effects of this medicine.

It is not known whether this medicine will harm an unborn baby. Tell your doctor if you are pregnant or plan to become pregnant while taking clonidine.

Clonidine can pass into breast milk and may harm a nursing baby. Tell your doctor if you are breast-feeding a baby.

Catapres is not approved for use by anyone younger than 18 years old. Do not give Kapvay to a child younger than 6 years old.

How should I take clonidine?

Take clonidine exactly as it was prescribed for you. Follow all directions on your prescription label. Your doctor may occasionally change your dose to make sure you get the best results. Do not take this medicine in larger or smaller amounts or for longer than recommended.

Clonidine is usually taken in the morning and at bedtime. If you take different doses of this medicine at each dosing time, it may be best to take the larger dose at bedtime.

Clonidine may be taken with or without food.

Do not use two forms of clonidine at the same time. This medicine is also available as a transdermal patch worn on the skin.

Do not crush, chew, or break an extended-release tablet. Swallow it whole. Tell your doctor if you have trouble swallowing the tablet.

If you need surgery, tell the surgeon ahead of time that you are using clonidine. You may need to stop using the medicine for a short time.

Do not stop using clonidine suddenly, or you could have unpleasant withdrawal symptoms. Ask your doctor how to safely stop using this medicine.

Call your doctor if you are sick with vomiting. Prolonged illness can make it harder for your body to absorb this medicine, which may lead to withdrawal symptoms. This is especially important for a child taking clonidine.

If you are being treated for high blood pressure, keep using this medication even if you feel well. High blood pressure often has no symptoms. You may need to use blood pressure medication for the rest of your life.

Store at room temperature away from moisture, heat, and light.

What happens if I miss a dose?

Take the missed dose as soon as you remember. Skip the missed dose if it is almost time for your next scheduled dose. Do not take extra medicine to make up the missed dose.

What happens if I overdose?

Seek emergency medical attention or call the Poison Help line at 1-800-222-1222.

Overdose symptoms may include dangerously high blood pressure (severe headache, pounding in your neck or ears, nosebleed, anxiety, chest pain, shortness of breath) followed by low blood pressure (feeling like you might pass out). Other overdose symptoms may include feeling cold, extreme weakness or drowsiness, weak or shallow breathing, pinpoint pupils, fainting, or seizure (convulsions).

What should I avoid while taking clonidine?

Avoid drinking alcohol. It may increase certain side effects of clonidine.

Clonidine may impair your thinking or reactions. Avoid driving or operating machinery until you know how this medicine will affect you. Dizziness or severe drowsiness can cause falls or other accidents.

Clonidine side effects

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

Call your doctor at once if you have:

  • severe chest pain, shortness of breath, irregular heartbeats;

  • a very slow heart rate;

  • severe headache, pounding in your neck or ears, blurred vision;

  • nosebleeds;

  • anxiety, confusion; or

  • a light-headed feeling, like you might pass out.

Serious side effects may be more likely in older adults.

Common clonidine side effects may include:

  • drowsiness, dizziness;

  • feeling tired or irritable;

  • dry mouth, loss of appetite;

  • constipation;

  • dry eyes, contact lens discomfort; or

  • sleep problems (insomnia), nightmares.

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 clonidine?

Taking this medicine with other drugs that make you sleepy can worsen this effect. Ask your doctor before taking clonidine with a sleeping pill, narcotic pain medicine, muscle relaxer, or medicine for anxiety, depression, or seizures.

Tell your doctor about all your current medicines and any you start or stop using, especially:

  • other heart or blood pressure medications;

  • an antidepressant; or

  • any other medicine that contains clonidine.

This list is not complete. Other drugs may interact with clonidine, including prescription and over-the-counter medicines, vitamins, and herbal products. Not all possible interactions are listed in this medication guide.

Further information

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

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

Copyright 1996-2020 Cerner Multum, Inc. Version: 9.01.

Medical Disclaimer

More about clonidine

  • Side Effects
  • During Pregnancy or Breastfeeding
  • Dosage Information
  • Patient Tips
  • Drug Images
  • Drug Interactions
  • Compare Alternatives
  • Support Group
  • Pricing & Coupons
  • 559 Reviews
  • Drug class: antiadrenergic agents, centrally acting
  • FDA Alerts (1)

Consumer resources

  • Clonidine Epidural Injection
  • Clonidine Extended-Release Tablets
  • Clonidine Tablets
  • Clonidine Patches
  • Clonidine Epidural (Advanced Reading)
  • … +2 more

Other brands: Catapres, Kapvay, Catapres-TTS, Duraclon, Nexiclon XR

Professional resources

  • Clonidine (AHFS Monograph)
  • … +6 more

Related treatment guides

  • Anxiety
  • ADHD
  • Alcohol Withdrawal
  • Atrial Fibrillation
  • … +19 more

Combination Antihypertensive Drugs: Recommendations for Use

Diuretics in Combination Antihypertensive Therapy

Diuretics are effective antihypertensive drugs. Treatment with a diuretic such as hydrochlorothiazide results in a dose-dependent blood pressure reduction that levels off with higher dosages (Table 2).11 In long-term trials, diuretics have been shown to reduce the incidence of stroke, congestive heart failure, coronary artery disease and total mortality from cardiovascular disease.


Blood Pressure Reductions Achieved with Hydrochlorothiazide Monotherapy

Dosage (mg per day) Blood pressure reduction (mm Hg)
Systolic Diastolic

Information from Neutel JM. Metabolic manifestations of low-dose diuretics. Am J Med 1996;101:71S–82S.


Dosage (mg per day) Blood pressure reduction (mm Hg)
Systolic Diastolic

Information from Neutel JM. Metabolic manifestations of low-dose diuretics. Am J Med 1996;101:71S–82S.

Unfortunately, the degree of improvement in cardiovascular mortality is less than would have been expected based on epidemiologic data. One postulated but not yet proven explanation is that the higher diuretic dosages used in the large trials cause relative hypokalemia, as well as increased serum lipid levels, insulin resistance and uric acid levels. These adverse metabolic effects counteract the positive cardiovascular benefits of blood pressure reduction. Such effects do not occur when diuretics are administered in a low dosage, such as 6.25 or 12.5 mg per day of hydrochlorothiazide.11

Because diuretics blunt the sodium- and water-retaining effects of many other antihypertensive drugs, they are the most commonly used medication in combination antihypertensive agents. The JNC VI states clearly, “If a diuretic is not chosen as the first drug, it is usually indicated as a second-step agent because its addition will enhance the effects of other agents.”1(p2429)


The discrepancy between the JNC VI recommendations for first-line use of thiazide diuretics and the actual use of these agents in clinical practice may be attributable to physicians’ concerns about the development of hypokalemia and hypomagnesemia, as well as the marketing of newer agents by pharmaceutical companies. Combination therapy with a potassium-sparing diuretic and a thiazide diuretic attempts to reduce the risk of adverse metabolic effects. Combination therapy does not obviate the need for serial monitoring of serum electrolyte levels, but it does decrease the incidence of thiazide-induced hypokalemia without an increased risk of hyperkalemia.12

Fixed-dose potassium-sparing–thiazide diuretic combinations have been in use for more than 20 years. Current combinations include spironolactone-hydrochlorothiazide (Aldactazide), triamterene-hydrochlorothiazide (Dyazide, Maxzide) and amiloride-hydrochlorothiazide (Moduretic). These combination drugs do not appear to differ significantly in efficacy or adverse effects.13 The described improvement in the bioavailability of Maxzide over Dyazide has not been shown to yield improved blood pressure control.14

All potassium-sparing–thiazide diuretic combinations seem to reduce blood pressure to the same degree as thiazide diuretics alone.15-18 In one large postmarketing surveillance study of patients treated with triamterene-hydrochlorothiazide,12 the incidence of hypokalemia was approximately one half to one third that expected in hydrochlorothiazide monotherapy. In addition, the amiloride-hydrochlorothiazide combination caused significantly less alteration of serum potassium levels than did hydrochlorothiazide given alone in dosages of 25 to 100 mg per day.15 The clinical applicability of the findings may be questionable because the studies used hydrochlorothiazide dosages that were significantly higher than those currently recommended.

The low dosages of hydrochlorothiazide (12.5 to 25 mg per day) advocated in the JNC VI provide significant blood pressure reduction while minimizing electrolyte abnormalities.19 It remains unclear whether the addition of a potassium-sparing agent confers additional benefit compared with a low dosage of hydrochlorothiazide alone.


Beta blockers cause retention of sodium and water. Diuretics can cause mild volume reduction that leads to an increase in renin secretion by the kidney. The rationale for combining beta blockers with diuretics is twofold: beta blockers blunt the increase in the plasma renin level that is induced by diuretics, and diuretics decrease the sodium and water retention that is caused by beta blockers.6,20

The combination of a beta blocker and a diuretic produces additive effects compared with monotherapy using either agent alone. A recent study21 assessed the safety and efficacy of antihypertensive therapy using the cardioselective beta blocker bisoprolol alone and in combination with low dosages of hydrochlorothiazide. The dosages of bisoprolol were 2.5, 5 and 10 mg per day. The hydrochlorothiazide dosages were 6.25 and 25 mg per day. The study showed that monotherapy with either agent was more effective than placebo, but that when combination therapy was used, the beneficial effects were greater than when either agent was used alone (Figure 1).21

Bisoprolol and Hydrochlorothiazide


Response of blood pressure to treatment with bisoprolol and hydrochlorothiazide (HCTZ).

Information from Frishman WH, Bryzinski BS, Coulson LR, DeQuattro VL, Vlachakis ND, Mroczek WJ, et al. A multifactorial trial design to assess combination therapy in hypertension. Treatment with bisoprolol and hydrochlorothiazide. Arch Intern Med 1994;154:1461–8 .


Response of blood pressure to treatment with bisoprolol and hydrochlorothiazide (HCTZ).

Information from Frishman WH, Bryzinski BS, Coulson LR, DeQuattro VL, Vlachakis ND, Mroczek WJ, et al. A multifactorial trial design to assess combination therapy in hypertension. Treatment with bisoprolol and hydrochlorothiazide. Arch Intern Med 1994;154:1461–8 .

In the same study,21 combination therapy was associated with a low incidence of adverse effects. Side effects for combined hydrochlorothiazide in a dosage of 6.5 mg per day and bisoprolol in all dosages included fatigue (9 percent of recipients), dizziness (6 percent), somnolence (3 percent), impotence (2 percent) and diarrhea (4 percent). When used in combination with bisoprolol, hydrochlorothiazide (6.25 mg) did not cause hypokalemia or any adverse effects on the lipid profile. Side effects increased with the use of higher dosages of bisoprolol or hydrochlorothiazide. The incidence of hypokalemia and hyperuricemia was greater for 25 mg per day of hydrochlorothiazide than for 6.25 mg per day. With higher bisoprolol dosages, the frequency and severity of asthenia, diarrhea, dyspepsia and somnolence increased significantly.


Angiotensin-converting enzyme (ACE) inhibitors are among the best tolerated antihypertensive drugs and have been used extensively as initial agents in the treatment of hypertension. The JNC VI1 recommends ACE inhibitors as second-line agents in most patients with hypertension and as first-line choices only in selected patients, including those with left ventricular systolic dysfunction and those with diabetes and microalbuminuria or proteinuria.

The reninangiotensin-aldosterone axis is important in the maintenance of systemic blood pressure. By causing volume and sodium depletion, thiazide diuretics stimulate the production of renin and angiotensin. This leads to a relative increase in blood pressure and sodium retention, which counteracts some of the other antihypertensive effects of the thiazide diuretics. ACE inhibitors interfere with the conversion of angiotensin I to angiotensin II and thereby decrease angiotensin II levels. These effects lead to decreased sodium retention and an enhanced antihypertensive effect.

Synergism between ACE inhibitors and diuretics is especially prominent in black patients, a population in whom monotherapy with ACE inhibitors has been shown to be less effective than it is in white patients. One small study22 of black patients with hypertension (N= 38) compared monotherapy using 20 mg per day of enalapril with combination therapy consisting of 20 mg of enalapril plus 12.5 mg of hydrochlorothiazide per day. Combination therapy significantly reduced systolic, diastolic and 24-hour ambulatory blood pressure measurements compared with monotherapy. Combination therapy controlled blood pressure to a level of less than 140/90 mm Hg in 74 percent of patients.

Studies have shown that ACE inhibitor–diuretic combinations achieve blood pressure control in approximately 80 percent of patients.20,23-25 Typical results were obtained in one of the larger double-blind, placebo-controlled trials.23

In this study,23 505 patients with diastolic blood pressures of 100 to 114 mm Hg received placebo, lisinopril (10 mg per day), hydrochlorothiazide (12.5 or 25 mg per day) or the combination of lisinopril (10 mg per day) and hydrochlorothiazide (12.5 or 25 mg per day). All drug therapies were more effective than placebo in lowering blood pressure, but the combination antihypertensive therapies produced the greatest effect (Figure 2).23

Lisinopril and Hydrochlorothiazide


Response of blood pressure to treatment with lisinopril and hydrochlorothiazide (HCTZ).

Information from Chrysant SG. Antihypertensive effectiveness of low-dose lisinopril-hydrochlorothiazide combination. A large multicenter study. Lisinopril-Hydrochlorothiazide Group. Arch Intern Med 1994;154:737–43.


Response of blood pressure to treatment with lisinopril and hydrochlorothiazide (HCTZ).

Information from Chrysant SG. Antihypertensive effectiveness of low-dose lisinopril-hydrochlorothiazide combination. A large multicenter study. Lisinopril-Hydrochlorothiazide Group. Arch Intern Med 1994;154:737–43.

No significant differences in blood pressure reduction were observed for the two dosages of hydrochlorothiazide, whether the drug was used alone or in a combination.23 Adverse metabolic effects were observed only for regimens containing hydrochlorothiazide in a dosage of 25 mg per day. Serum potassium levels were significantly lower only for monotherapy with 25 mg per day of hydrochlorothiazide. Serum glucose measurements increased with the 25-mg dosage used as monotherapy or in combination with lisinopril.

The study23 found that the combination consisting of 10 mg per day of lisinopril and 12.5 mg per day of hydrochlorothiazide was well tolerated. The most commonly observed side effects were pharyngitis (14 percent of recipients), increased cough (6 percent), dizziness (2 percent), headache (12 percent) and asthenia (4 percent). Cough was the only side effect that was more prevalent in this group than in the placebo group.

Based on this large study,23 antihypertensive drug combinations containing an ACE inhibitor and a lower dose of hydrochlorothiazide are more desirable. It is important to be aware that the doses of ACE inhibitor in the antihypertensive drug combinations do not reach the target doses of ACE inhibitors recommended for the treatment of congestive heart failure, which may be a limitation in these patients.26


In patients for whom ACE inhibitor–diuretic combinations are indicated but not tolerated because of cough, angiotensin-II receptor antagonist–diuretic combinations are available. Angiotensin-II receptor antagonists work by blocking specific angiotensin II subtype I, thereby selectively inhibiting the vasoactive properties of angiotensin II.

One study27 evaluated the efficacies of losartan in a dosage of 50 mg per day, hydrochlorothiazide in a dosage of 12.5 mg per day and combination therapy with 50 mg per day of losartan and 6.25 or 12.5 mg per day of hydrochlorothiazide. The treatments were compared with each other and with placebo (Figure 3).27 The greatest antihypertensive effect occurred with the combination of 50 mg of losartan and 12.5 mg of hydrochlorothiazide. This treatment reduced diastolic blood pressure to less than 90 mm Hg (or a reduction of 10 mm Hg or greater) in 78 percent of patients. The combination of losartan with the lower hydrochlorothiazide dose (6.25 mg) demonstrated no benefit over monotherapy with losartan. No significant differences in adverse events were attributable to the combination of losartan (50 mg) and hydrochlorothiazide (12.5 mg) compared with placebo.

Losartan and Hydrochlorothiazide


Response of blood pressure to treatment with losartan and hydrochlorothiazide (HCTZ).

Information from MacKay JH, Arcuri KE, Goldberg AI, Snapinn SM, Sweet CS. Losartan and low-dose hydrochlorothiazide in patients with essential hypertension. A double-blind, placebo-controlled trial of concomitant administration compared with individual components. Arch Intern Med 1996;156:278–85.


Response of blood pressure to treatment with losartan and hydrochlorothiazide (HCTZ).

Information from MacKay JH, Arcuri KE, Goldberg AI, Snapinn SM, Sweet CS. Losartan and low-dose hydrochlorothiazide in patients with essential hypertension. A double-blind, placebo-controlled trial of concomitant administration compared with individual components. Arch Intern Med 1996;156:278–85.

Clonidine Prevents Insulin Resistance and Hypertension in Obese Dogs

The mechanism involved in the pathogenesis of the increased blood pressure in obesity is incompletely understood. Studies in our laboratory12 and by others3 suggest that insulin resistance may be the link between obesity and hypertension. However, other observations suggest that the relation between insulin and obesity-induced hypertension is not so straightforward. The San Antonio Heart Study showed that hyperinsulinemia is more common in Mexican Americans than in white non-Hispanics, yet the prevalence of hypertension is high in the latter group.4 Hall et al5 failed to observe an increase in blood pressure when normal dogs were given a chronic infusion of insulin with or without norepinephrine.

We believe that an alternate hypothesis to explain the pathogenesis of obesity-induced hypertension is that chronic central sympathetic nervous system activation links insulin resistance and hypertension. Sowers et al6 observed that borderline hypertensive obese subjects had higher norepinephrine levels than did nonobese normotensive control subjects, that their blood pressure correlated with norepinephrine levels, and that weight loss was accompanied by a fall in blood pressure that correlated with a decrease in serum norepinephrine. Hall et al7 suggested that combined α- and β-adrenergic blockade reduced arterial pressure to a much greater extent in obese than in normal dogs. Fasting or caloric deprivation reduces sympathetic activity and overfeeding stimulates sympathetic activity.8

Diebert and DeFronzo9 demonstrated that impairs both peripheral and hepatic resistance to the action of insulin. Jamerson et al10 demonstrated that a reflex increase in sympathetic tone in normotensive individuals can lead to acute insulin resistance in the forearm.

Thus, it is possible that central activation of the sympathetic nervous system is the physiological link that connects excess dietary intake to insulin resistance and hypertension. Through the feeding of fat with or without clonidine to dogs, the present study was designed to evaluate the role that the central sympathetic system plays in the development of hypertension and insulin resistance.


Thirteen adult mongrel dogs (6 males and 7 females) were trained to stand quietly in a padded sling and were surgically instrumented with 1 ascending aortic and 2 right atrial catheters. The dogs recovered for 3 weeks before baseline measurements were made. Dogs were randomly assigned to either a high-fat-diet, no-clonidine group (n=6) that received the control diet (1 can of dog food ) for 2 weeks followed by 6 weeks of a high fat diet consisting of 0.8 kg of cooked beef fat in addition to the regular diet2 or a high-fat-diet, clonidine group (n=7) that received 0.3 mg clonidine PO BID initiated 1 week before the start of the high fat diet and continued with the fat diet for an additional 6 weeks. (Figure 1) All dogs received vitamin supplements (VAL Syrup; Fort Dodge Laboratories) and antibiotics throughout the entire study. Dogs were housed in air-conditioned cages and fed between 1:00 and 3:00 pm each day. Blood pressure, heart rate, and body weight were measured daily. Cardiac output, plasma glucose, and insulin were measured twice a week. All measurements were made between 8:00 and 11:00 am and before the daily feeding. All the procedures in this study were in accordance with the University of Minnesota, Northwestern University, and University of Michigan guidelines on animal experimentation.

Laboratory Measurements

Arterial pressure was measured with a pressure transducer mounted at the level of the heart, and the analog signals were sent to a computer to be analyzed. The computer calculated the average systolic, diastolic, and mean blood pressures and heart rate (over a 15- to 30-minute period). Cardiac output was measured with Cardiogreen dye (Waters Instruments).

Insulin resistance was assessed with a multiple insulin dose euglycemic hyperinsulinemic clamp. The multiple insulin infusion euglycemic clamps were performed twice before starting the high fat diet and at 1, 3, and 6 weeks of the high fat diet. Arterial samples were obtained to determine basal glucose, insulin, and potassium levels, and cardiac output was measured. A constant infusion of insulin was administered at 3 insulin infusion rates (1, 2, and 30 mU · kg−1 · min−1).1 Concomitant with the insulin, an intravenous infusion of 20% glucose was administered with a variable infusion syringe pump to maintain euglycemia. To prevent severe hypokalemia, K2HPO4 was infused. Blood pressure and heart rate were continuously monitored throughout the clamp procedure. During the last 30 minutes of the insulin infusion, arterial blood was sampled for glucose, insulin, and potassium levels, and cardiac output was measured as the average of 2 determinations.

In 4 no-clonidine fat–fed dogs and 4 clonidine plus fat–fed dogs, basal glucose turnover was measured (at weeks 0, 1, 3, and 6) using d-glucose.11 The rate of hepatic glucose production was calculated, assuming steady-state conditions, using the Steele equation. These values of basal glucose production were used in the calculation of the insulin dose-response curves.

Analytic Methods

The serum glucose concentration was measured in duplicate with the glucose oxidase method using a glucose analyzer (model A23; Yellow Springs Instruments). Serum insulin was measured with double-antibody radioimmunoassay (ICN Biomedical). Plasma electrolytes were measured with flame photometry. Blood for the determination of plasma glucose specific activity was collected in sodium fluoride–treated tubes and immediately spun, and the supernatant was removed and stored at −20°C.1

Statistical Analysis

All values are mean±SEM. Weekly blood pressures, heart rates, and body weights were determined by averaging the daily values, and cardiac output and plasma glucose and insulin levels were determined by averaging the 2 values obtained each week. The dose-response curves for whole body glucose uptake versus insulin were fitted to a 4-parameter logistic equation using a least-squares mean iterative routine (ALLFIT)12 as follows: Y={(A−D)/}+D, where A is the expected maximal response, D is the expected minimal response, I is the insulin concentration, ED50 is the insulin concentration with expected response halfway between A and D, and B is the slope factor. After obtaining parameters A, D, B, and ED50 for the fat and no clonidine and the fat plus clonidine groups, separate analyses were performed to test whether parameters were similar between the groups. A repeated measures analysis was used to determine whether a significant change in the parameters occurred over time.

Within each group, a repeated measures ANOVA was performed for each variable to determine whether a significant change in the variable occurred over time. A 2-factor ANOVA for repeated measures was then performed for each variable to assess differences between the dogs fed the high fat diet and no clonidine and the dogs fed clonidine plus the high fat diet.


Hemodynamic, Hormonal, and Metabolic Data

During the 1-week control period and the 1 week of clonidine plus regular diet, no significant differences were noted between the 2 groups for any of the measured variables. Over the 6 weeks of the high fat diet, both the clonidine and no-clonidine groups increased their body weight (P<0.001) Table 1. In the high fat diet group without clonidine, the gain in weight was associated with a significant increase in arterial pressure (P<0.001), heart rate (P<0.001), and cardiac output (P<0.01). The clonidine plus fat–fed dogs experienced no change in these hemodynamic parameters (Table 1). Plasma glucose did not significantly increase in either group with feeding of the high fat diet; however, we observed only in the group that did not receive clonidine a significant increase in fasting serum insulin concentration (86±10 to 208±21 pmol/L, P<0.001).

Euglycemic Clamp Data

During the euglycemic clamp studies, the steady-state blood glucose concentration in all dogs averaged ∼5.2 mmol/L and did not differ from the fasting concentration at any insulin infusion rate. The coefficient of variation of glucose level at each insulin plateau was<5%.

To characterize the ability of clonidine treatment to alter the insulin-mediated glucose uptake relation that occurs in dogs fed a high fat diet, we measured insulin-mediated glucose uptake dose-response curves before and after the high fat diet. Basal rates of whole body glucose uptake (hepatic glucose production) were measured on 4 dogs in the clonidine group and 4 dogs in the no-clonidine group. The high fat diet did not significantly change basal rates of whole body glucose uptake in either group of dogs (24±6 μmol · kg −1 · min−1 at week 0 versus 22±8 μmol · kg−1 · min−1 at week 6 in the no-clonidine group and 26±8 μmol · kg−1 · min−1 at week 0 versus 25±9 μmol · kg−1 · min−1 at week 6 in the clonidine group). Throughout the study, the 1–mU · kg−1 · min−1 insulin dose completely suppressed hepatic glucose output in both groups of dogs. During increasing insulin dose rates, whole body glucose uptake increased in a sigmoidal fashion (Figure 2). In the no-clonidine group, the high fat diet was associated with a shift in the glucose uptake curve to the right, and the rate of maximal whole body glucose uptake was significantly decreased (P<0.001) (Table 2). Compared with the control, pre–high fat period, the insulin concentration expected to produce a half-maximal response in glucose uptake (insulin ED50 dose) was 50% (P<0.01) higher at 1 week and 85% (P<0.001) higher at 6 weeks of the fat diet. In contrast to the no-clonidine group, the clonidine-treated group did not experience any change in the glucose uptake curve during the 6 weeks of the high fat diet. After 6 weeks of the high fat diet, the clonidine group had both maximal glucose uptake and the insulin concentration expected to produce a half-maximal response in glucose uptake (insulin ED50 dose), which were unchanged from values obtained in this control period. (Table 2) In addition, 1 week of clonidine treatment without the high fat diet (week −1 versus week 0) also did not change the insulin-mediated glucose uptake curve. Finally, despite the infusion of the same amount of insulin per kilogram of weight in both groups of dogs, only the group of dogs that did not receive clonidine experienced, when fed the high fat diet, an increase over time in the plateau insulin values during the multiple-dose clamps (Table 2).

In the no-clonidine group, the high fat diet was associated with an increase in resting cardiac output (P<0.01), whereas in the clonidine-treated group, the high fat diet resulted in no significant increase in cardiac output (P>0.1) (Table 1). In both groups of dogs, before starting the high fat diet, euglycemic hyperinsulinemia caused a dose-dependent increase in cardiac output (Figure 3). In the no-clonidine group, feeding the high fat diet resulted in rightward shift of the effect of insulin to increase cardiac output and a reduced maximal insulin-stimulated cardiac output (P<0.05) (Table 2). After 6 weeks of the fat diet, euglycemic hyperinsulinemia caused virtually no increase in cardiac output. However, in the clonidine group, the high fat diet did not change the ability of insulin to increase cardiac output. After 6 weeks of the high fat diet, euglycemic hyperinsulinemia in clonidine-treated dogs still resulted in a 37% increase in cardiac output.

In both groups of dogs, before starting the high fat diet, the euglycemic clamp resulted in a 6±2 mm Hg decrease in arterial pressure and a 7±3 bpm increase in rate. In the no-clonidine group, after 6 weeks of a high fat diet, euglycemic hyperinsulinemia did not cause either a decrease in arterial pressure or an increase in heart rate; however, in the clonidine group, the high fat diet euglycemic hyperinsulinemia was still associated with a 5±2 mm Hg decrease in pressure and a 5±3 increase in heart rate.


The present study demonstrates that clonidine, an antihypertensive agent that lowers blood pressure through stimulation of central α2-receptors and, to a lesser degree, the I1 imidazole receptors, prevented both the hypertension and insulin resistance associated with weight gain in the dog. Our finding that clonidine prevented hypertension in the obese dog model is consist with the report of Hall et al7 They demonstrated that combined α- and β-adrenergic blockade reduced arterial pressure to a much greater extent in obese than in normal dogs. We believe the mechanism whereby clonidine treatment prevented the increase in blood pressure associated with weight gain is due to central inhibition of the peripheral sympathic nervous system.13 Because we did not directly measure sympathetic activity, further studies are necessary to directly prove that clonidine inhibited peripheral sympathetic activity. The failure of weight gain to induce tachycardia in the clonidine-treated dogs is consistent with the known central nervous system action of clonidine. In addition, the failure of clonidine-treated dogs to increase their cardiac output in association with weight gain is consistent with a reduced degree of renal salt and water retention. Kassab et al14 have shown that bilateral renal denervation prevents the hypertension and sodium retention associated with obesity in the dog. We believe that clonidine treatment could have prevented the high fat diet–induced activation of the renal efferent sympathetic nerves. Further studies that measure in detail the sodium and fluid balance in clonidine-treated dogs fed a high fat diet will be necessary to more directly answer whether clonidine does prevent sodium and fluid retention in obese dogs.

Perhaps the more important and new finding in the present study is that clonidine also prevented the insulin resistance associated with obesity in the dog. Using the multiple insulin dose euglycemic clamp, we demonstrated that clonidine prevents the reduced sensitivity and responsiveness of the insulin-mediated glucose uptake dose-response curve that is associated with weight gain (Figure 2, Table 2). It has been speculated that insulin resistance (ie, resistance to the ability of insulin to stimulate glucose uptake) is the common metabolic abnormality connecting obesity, hypertension, and increased sympathetic nervous system activity. This hypothesis is supported by numerous reports that document a relation between insulin resistance and hypertension.123 However, the present study supports the concept, originally proposed by Julius et al,15 that central nervous system–induced sympathetic activation, not insulin resistance or hyperinsulinemia, is the metabolic link that connects obesity to hypertension.

Our finding that clonidine treatment prevented the insulin resistance associated with weight gain in the dog is consistent with other reports. Giugliano et al16 reported that in 20 hypertensive patients with non–insulin-dependent diabetes mellitus, clonidine treatment was associated with an improvement in insulin sensitivity in peripheral tissues. Using the glucose clamp, these investigators found that clonidine significantly improved overall glucose metabolism and that this improvement was accompanied by increases in both oxidative and nonoxidative glucose metabolism. Other central acting antihypertensive drugs also have been reported to improve insulin resistance. Moxonidine, a highly selective I1 imidazole receptor agonist with weak central α2-receptor effects, has been shown to prevent the insulin resistance, hyperinsulinemia, and hypertension in rats fed a fructose-enriched diet17 and to reduce blood pressure, reduce triglycerides, and improve glucose tolerance in obese spontaneously hypertensive rats.18 However, in their fructose-fed rate model, Hwang et al19 failed to show a beneficial effect of clonidine in preventing insulin resistance despite demonstrating that clonidine did prevent the increase in blood pressure. The acute administration of clonidine has been shown to induce hyperglycemia and impaired glucose tolerance in rats and humans.20 However, chronic clonidine treatment does not appear to exert such effects.21

The present study was not designed to determine the mechanism whereby clonidine prevents the development of insulin resistance that occurs in dogs fed a high fat diet. However, because of previous studies and our present study design, some inferences can be made into the mechanism of insulin resistance. Insulin-mediated glucose uptake is determined both by the ability of insulin to stimulate glucose extraction at the level of tissues and cells and by the rate of glucose and insulin delivery (blood flow). Thus, the relative contributions of tissue and blood flow actions of insulin will determine the overall rate of glucose uptake (ie, degree of insulin resistance). Baron et al22 observed that the reduced rate of insulin-mediated glucose uptake that occurs in non–insulin-dependent diabetes mellitus, obesity, and hypertension may be due in large part to an impairment in the action of insulin to increase skeletal muscle blood flow. In the present and other studies,1 we have demonstrated that obese dogs have a reduced ability of euglycemic hyperinsulinemia to increase cardiac output (Figure 3). Because clonidine treatment enabled euglycemic hyperinsulinemia to cause a dose-dependent increase in cardiac output even after the dogs gained weight, we believe that the increased blood flow responses to insulin may have contributed to the improvement in insulin resistance with clonidine. Vollenweider et al23 demonstrated that insulin resistance in obese subjects is associated, in skeletal muscle, with a specific impairment of sympathetic neural and vasodilatory responsiveness to hyperinsulinemia. The impairment of insulin to increase skeletal muscle blood flow in obesity and in non–insulin-dependent diabetes is speculated to be related to an abnormality in the nitric oxide system.24 Insulin is known to interact with the sympathetic nervous system at the vascular level, predominantly through the α2-adrenergic pathway.25 Lacolley et al26 demonstrated that the sympathetic nervous system plays an important role in modulating the synthesis, release, or both of vascular nitric oxide. Thus, it is possible that clonidine treatment of dogs fed a high fat diet may have prevented insulin resistance by blocking the sympathetically mediated reduced vasodilator responsiveness to insulin known to occur in obesity.

Besides the affect of the sympathetic nervous system on glucose uptake by reducing blood flow, there is evidence that the sympathetic nervous system can directly influence the cellular uptake of glucose. Takahashi et al27 demonstrated in the rat that ventromedial hypothalamic stimulation can alter peripheral glucose uptake at the cellular level. Catecholamine treatment of rat adipocytes has also been demonstrated to reduce the tyrosine kinase activity of the insulin receptor.28 Finally, because clonidine is known to suppress free fatty acid levels,29 it is possible that glucose uptake in our obese dogs was improved by increasing oxidative glucose metabolism.

In summary, the results of the present study document that clonidine treatment of dogs fed a high fat diet blocks the development of both hypertension and insulin resistance even though the dogs still gained weight. Further studies will be necessary to better clarify how clonidine is able to dissociate weight gain from both hypertension and insulin resistance.

Figure 1. Schematic representation of the study design of the project.

Figure 2. Rates of whole body insulin-mediated glucose uptake (M) determined during euglycemic clamp studies over a wide range of steady-state insulin concentrations (□, week 0; ▵, week 1 of fat diet; X, week 6 of fat diet) in dogs fed a high fat diet with and without clonidine treatment. Weight gain resulted in a shift to the right and a decrease in the maximal rate of M (P<0.001) in dogs not treated with clonidine; however, if the dogs were treated with clonidine, weight gain did not alter the dose-response relation.

Figure 3. Insulin-induced changes in cardiac output were determined during euglycemic clamp studies over a wide range of steady-state insulin concentrations (□, week 0; ▵, week 1 of fat diet; X, week 6 of fat diet) in dogs fed a high fat diet with and without clonidine. In the absence of clonidine, weight gain resulted in an increase in basal cardiac output and a shift to the right of the effect of insulin to increase cardiac output (P<0.01); however, with clonidine treatment, weight gain was not associated with either an increase in cardiac output or a shift in the effect of insulin to increase cardiac output.

BP indicates mean arterial pressure; HR, heart rate; and CO, cardiac output.

1P<0.001 and

2P<0.01, control period vs 6 weeks of 8 high fat or control diet.

3P<0.01, clonidine vs no-clonidine group.

Table 2. Maximal and ED50 Values for Insulin-Mediated Glucose Uptake, Basal Maximal and ED50 Values for Cardiac Output, and Plateau Insulin Concentrations in High-Fat Clonidine-Fed and High Fat Non–Clonidine-Fed Dogs

Week 0 Week 1 Week 3 Week 6
No Clonidine Clonidine No Clonidine Clonidine No Clonidine Clonidine No Clonidine Clonidine
Whole body glucose uptake, μmol · kg · −1min−1
Maximum 104±15 104 ±19 79±14 99±182 72±15 101±193 70 ±16 102±183
ED50 695±24 673 ±21 1048±32 676±293 1343±42 684±253 1292 ±72 684±213
Cardiac output, L/min
Maximum 4.9±.3 4.9±.3 4.6 ±0.3 4.7±0.3 4.2±0.3 5.0±0.21 4.6±0.3 4.8 ±0.32
Basal 3.2±0.4 3.3±0.4 3.5 ±0.3 3.3±0.5 3.6±0.3 3.4±0.41 4.5±0.5 3.5 ±0.32
ED50 425±25 435±26 763 ±21 440±173 1134±27 443±243 1213±27 438 ±173
Plateau insulin concentration, pmol/L
1 mU · kg−1 · 1 min−1 359±28 358±28 579±2523 365 ±21 652±2223 360±18 649±2423 356±19
2 mU · kg−1 · 1 min−1 727±57 701±43 886±6423 721 ±45 937±6123 719±45 978±5823 716±41
3 mU · kg−1 · 1 min−1 16 277±94 16 257±89 17 240 ±9823 16 298±89 17 745±9923 16 321 ±79 17 839±9923 16 278±83

Maximum indicates whole body glucose uptake and cardiac output at maximally effective insulin concentrations; ED50, whole body glucose uptake and cardiac output at the insulin concentration (pmol/L) at which half-maximum is achieved; and Basal, resting values of cardiac output just before starting the euglycemic hyperinsulinemic clamps.

All values of glucose uptake and cardiac output are derived from curve-fitting analysis (ALLFIT) using a four-parameter logistic equation on the basis of group mean values.


2P<0.01, and

3P<0.001, clonidine group vs no-clonidine group.

This work was supported in part by National Institutes of Health grant 1RO1-HL-52205.


Correspondence to Albert P. Rocchini, MD, Pediatric Cardiology, C.S. Mott Hospital, University of Michigan Medical Center, F1310 MCHC, Box 0204, 1500 East Medical Center Dr, Ann Arbor, MI 48109-0204. E-mail

  • 1 Rocchini AP, Marker P, Cervenka T. Time course of insulin resistance associated with feeding dogs a high-fat diet. Am J Physiol.1997; 272:E147–E154.MedlineGoogle Scholar
  • 2 Rocchini AP, Moorehead CS, DeRemer S, Bondie D. Pathogenesis of weight-related changes in pressure in the dog. Hypertension.1989; 13:922–928.Google Scholar
  • 3 O’Hare JA. The enigma of insulin resistance and hypertension, insulin resistance, blood pressure and the circulation. Am J Med.1988; 84:505–510.CrossrefMedlineGoogle Scholar
  • 4 Ferrannini E, Haffner SM, Stern MP. Essential hypertension: an insulin-resistance state. J Cardiovasc Pharmacol. 1990;15(suppl 5):S18–S25.Google Scholar
  • 5 Hall JE, Brands MW, Kivlighn SD, Mizelle HL, Hidebrandt DA, Gaillard CA. Chronic hyperinsulinemia and blood pressure: interaction with catecholamines? Hypertension.1990; 15:519–527.Google Scholar
  • 6 Sowers JR, Nyby M, Stern N, Beck F, Baron S, Catania R, Vlachis N. Blood pressure and hormonal changes associated with weight reduction in the obese. Hypertension.1982; 4:686–691.Google Scholar
  • 7 Hall JE, Van Vliet BN, Garrity CA, Connell RD, Brands MW. Role of increased adrenergic activity in obesity-induced hypertension. Circulation. 1992;86(suppl I):I-541. Abstract.Google Scholar
  • 8 Young JB, Saville ME, Rothwell NJ, Stock MJ, Landsberg L. Effect of diet and cold exposure on norepinephrine turnover in brown adipose tissue in the rat. J Clin Invest.1982; 69:1061–1071.CrossrefMedlineGoogle Scholar
  • 9 Diebert DC, DeFronzo RA. Epinephrine-induced insulin resistance in man. J Clin Invest.1980; 65:717–721.CrossrefMedlineGoogle Scholar
  • 10 Jamerson KA, Julius A, Gudbrandsson T, Andersson O, Brant DO. Reflex sympathetic activation induces acute insulin resistance in the human forearm. Hypertension.1993; 21:618–623.Google Scholar
  • 11 Finegood DT, Bergman RN, Vranic M. Estimation of endogenous glucose production during hyperinsulinemic euglycemic glucose clamps: comparison of unlabeled and labeled exogenous glucose infusates. Diabetes.1987; 36:914–924.CrossrefMedlineGoogle Scholar
  • 12 DeLean A, Munson PJ, Rodbard D. Simultaneous analysis of families of sigmoidal curves: application to bioassay, radioligand assay and physiological dose-response curves. Am J Physiol.1978; 235:E97–E102.CrossrefMedlineGoogle Scholar
  • 13 Van Zwieten PA. Centrally acting antihypertensives: a renaissance of interest. Mechanisms and haemodynamics. J Hypertens.1997; 15:S3–S8.CrossrefMedlineGoogle Scholar
  • 14 Kassab S, Kato T, Wilkins FC, Chen R, Hall JE, Granger JP. Renal denervation attenuates the sodium retention and hypertension associated with obesity. Hypertension.1995; 25:893–897.CrossrefMedlineGoogle Scholar
  • 15 Julius S, Gudbrandsson T, Jamerson K, Shahab ST, Andersson O. The hemodynamic link between insulin resistance and hypertension. J Hypertens.1991; 9:983–986.CrossrefMedlineGoogle Scholar
  • 16 Giugliano D, Acampora R, Marfella R, La Marca C, Marfella M, Nappo F, D’Onofrio F. Hemodynamic and metabolic effects of transdermal clonidine in patients with hypertension and non-insulin-dependent diabetes mellitus. Am J Hypertens.1998; 11:184–189.CrossrefMedlineGoogle Scholar
  • 17 Rosen P, Ohly P, Gleochman J. Experimental benefit of moxonidine on glucose metabolism and insulin secretion in the fructose-fed rat. J Hypertens. 1997;15(suppl I):S31–S38.Google Scholar
  • 18 Ernsberger P, Friedman JE, Kooletsky RJ. The I1-imidazoline receptor: from binding site to therapeutic target in cardiovascular disease. J Hypertens. 1997;15(suppl I):S9–S23.Google Scholar
  • 19 Hwang I, Ho H, Hoffman B, Reaven G. Fructose-induced insulin resistance and hypertension in rats. Hypertension.1987; 10:512–516.Google Scholar
  • 20 Metz SA, Halter JB, Robertson RP. Induction of defective insulin secretion and impaired glucose tolerance by clonidine. Diabetes.1978; 27:554–562.CrossrefMedlineGoogle Scholar
  • 21 Barbieri C, Caldara R, Testori G, Pierpoli V, Trezzi R, Romussi M, Ferrari C. Oral glucose tolerance and insulin response after one week’s clonidine treatment in hypertensive patients. ActaDiabetol Lantina.1981; 18:59–63.Google Scholar
  • 22 Baron AD, Laakso M, Brechtel G, Edelman SV. Mechanism of insulin resistance in insulin-dependent diabetes mellitus: a major role for reduced skeletal muscle blood flow. J Clin Endocrinol Metab.1991; 73:637–643.CrossrefMedlineGoogle Scholar
  • 23 Vollenweider P, Randin B, Tappy L, Jequier E, Nicod P, Scherrer U. Impaired insulin-induced sympathetic neural activation and vasodilation in skeletal muscle in obese humans. J Clin Invest.1994; 93:2365–2371.CrossrefMedlineGoogle Scholar
  • 24 Steinberg HO, Brechtel G, Johnson A, Fineberg N, Baron AD. Insulin-mediated skeletal muscle vasodilation is nitric oxide dependent: a novel action of insulin to increase nitric oxide release. J Clin Invest.1994; 94:1172–1179.CrossrefMedlineGoogle Scholar
  • 25 Lembo G, Iaccarino G, Vecchione C, Barbato E, Izzo R, Fontana D, Trimarco B. Insulin modulation of an endothelial nitric oxide component present in the alpha2- and beta-adrenergic responses in human forearm. J Clin Invest.1997; 100:2007–2014.CrossrefMedlineGoogle Scholar
  • 26 Lacolley PJ, Lewis SJ, Brody MJ. Role of sympathetic nerve activity in the generation of vascular nitric oxide in urethane-anesthetized rats. Hypertension.1991; 17:881–887.Google Scholar
  • 27 Takahashi A, Sudo M, Minokoshi Y, Shimazua T. Effect of ventromedial hypothalamic stimulation on glucose transport system in rat tissue. Am J Physiol.1992; 263:R1228–R1234.MedlineGoogle Scholar
  • 28 Haring HU, Kirsch D, Obermaier B, Ermel B, Machicaco F. Reduced tyrosine kinase activity of insulin receptor isolated from rat adipocytes rendered insulin resistant by catecholamine treatment in vitro. Biochem J.1986; 234:59–66.CrossrefMedlineGoogle Scholar
  • 29 Swislocki ALM, Vestal RE, Reaven GM, Hoffman BB. Acute metabolic effects of clonidine and adenosine in man. Horm Metab Res.1993; 25:90–95.CrossrefMedlineGoogle Scholar

The Best Diet Pill for Fast Weight Loss | Clonidine Weight Loss

p57 hoodia slimming pills clonidine weight loss Independent Review Weight Loss p57 slimming capsule . . . . reginae carter weight loss Independent Review healthy veg recipes for weight loss . clonidine weight loss . . . diet pills diethylpropion .
chinese diet supplement . clonidine weight loss . . . . . clonidine weight loss . clonidine weight loss . mushroom weight Topical monica lewinsky weight loss clonidine weight loss loss pills . . clonidine weight loss . clonidine weight loss . clonidine weight loss . clonidine weight loss . australian approved weight loss pills . weight loss for short women . . . weight loss diets that work clonidine weight loss fast for free . . clonidine weight clonidine weight loss loss . . thermo shock fat burner side effects . . kathrine herzer weight loss . . clonidine weight loss . . olive oil in the morning for weight loss . fat binder carb blocker appetite reducer . . . pharmacist gave wrong pills to lose weight .
clonidine weight loss . clonidine weight loss . . swanson fat burner . . . . 5htp weight loss . strongest prescription diet pill . comments on best weight loss pills to use . clonidine weight loss . clonidine weight loss . weight loss is a symptom clonidine weight loss of . . fluid pills weight loss . clonidine weight loss . clonidine weight loss . clonidine weight loss . clonidine weight loss . weight loss massachusetts . first lose weight then build muscle . clonidine weight loss . weight loss recourses . clonidine weight loss p57 hoodia slimming pills Top 5 Best Best Reviews p57 slimming capsule.

  • daily gym workout for weight loss
  • weight loss boise
  • nature driven appetite suppressant
  • constipation pills for weight loss
  • Clonidine for Tourette’s syndrome, ADHD and sleep-onset disorder

    This leaflet is about the use of clonidine for Tourette’s syndrome, attention-deficit hyperactivity disorder (often shortened to ADHD) and sleep-onset disorder (difficulty getting to sleep).

    This leaflet has been written for parents and carers about how to use this medicine in children. Our information sometimes differs from that provided by the manufacturers, because their information is usually aimed at adult patients. Please read this leaflet carefully. Keep it somewhere safe so that you can read it again.

    Do not stop giving clonidine suddenly, as your child’s blood pressure may become dangerously high.

    Name of drug

    Brand names: Catapres®

    Many generic (unbranded) versions are also available.

    Why is it important to take this medicine?

    • For children with Tourette’s syndrome, clonidine will help to reduce the severity and frequency of tics.
    • For children with ADHD, clonidine helps to reduce hyperactive symptoms.
    • For children with sleep disorders and difficulty getting to sleep, clonidine will help them fall asleep.

    What is clonidine available as?

    • Catapres® tablets: 100 micrograms; these contain gelatine and lactose
    • Generic (non-branded) tablets: 25 micrograms; these contain lactose
    • Liquid medicine can be ordered specially from your pharmacist

    When should I give clonidine?

    For Tourette’s syndrome and ADHD, clonidine is usually given once a day to start with. This can be in the morning OR the evening.
    Your doctor may then suggest that you give it two or three times a day, depending on how much your child needs.

    • Twice each day: this is once in the morning and once in the evening. Ideally, these times are
    • 10–12 hours apart, for example some time between 7 am and 8 am, and between 7 pm and 8 pm.
    • Three times a day: this should be first thing in the morning, early afternoon (e.g. after school) and at bedtime. Ideally, these times are at least 4 hours apart.

    For sleep disorders, clonidine is given once a day, about an hour before bedtime.

    Give the medicine at about the same time(s) each day so that this becomes part of your child’s daily routine, which will help you to remember.

    How much should I give?

    Your doctor will work out the amount of clonidine (the dose) that is right for your child. The dose will be shown on the medicine label.

    It is important that you follow your doctor’s instructions about how much to give.

    How should I give it?

    Tablets should be swallowed with a glass of water, milk or juice. Your child should not chew the tablet.

    You can crush the tablet and mix it with a small amount of soft food such as yogurt, honey or jam. Make sure your child swallows it straight away, without chewing.

    Liquid medicine: Measure out the right amount using an oral syringe or medicine spoon. You can get these from your pharmacist. Do not use a kitchen teaspoon as it will not give the right amount.

    When should the medicine start working?

    The medicine should start to work within about 45 minutes of giving it.

    What if my child is sick (vomits)?

    • If your child is sick less than 30 minutes after having a dose of clonidine, give them the same dose again.
    • If your child is sick more than 30 minutes after having a dose of clonidine you do not need to give them another dose. Wait until the next normal dose.

    If your child is sick again, seek advice from your GP, pharmacist or hospital. They will decide what to do based on your child’s condition and the specific medicine involved.

    What if I forget to give it?

    If you usually give it once a day in the morning
    Give the missed dose when you remember during the day, as long as this is at least 12 hours before the next dose is due.

    If you usually give it once a day in the evening
    If you remember before bedtime, give the missed dose. If you remember after this, you do not need to wake your child up to give them the missed dose. If your child is taking clonidine for Tourette’s syndrome or ADHD, you can give the missed dose in the morning, as long as this is at least 12 hours before the next evening dose is due. If your child has clonidine for sleep disorders, you should NOT give the missed dose in the morning.

    If you usually give it twice a day
    If you remember up to 4 hours after you should have given a dose, give your child the missed dose. For example, if you usually give a dose at about 7 am, you can give the missed dose at any time up to 11 am. If you remember after that time, do not give the missed dose. Wait until the next normal dose.

    If you usually give it three times a day
    Do not give the missed dose. Give the next dose as normal.

    Never give a double dose of clonidine. If you have missed more than one dose, contact your doctor for advice.

    What if I give too much?

    It may be dangerous to give too much clonidine, as it may make your child’s blood pressure very low (your child will feel dizzy and may faint). If you think you may have given your child too much, contact your doctor or local NHS services (111 in parts of England and Scotland; 0845 46 47 in Wales) or take your child to hospital.

    Take the medicine container or packet with you, even if it is empty. This will be useful to the doctor. Have the medicine package with you if you telephone for advice.

    Are there any possible side-effects?

    We use medicines to make our children better, but sometimes they have other effects that we don’t want (side-effects).

    • Your child may have a dry mouth, feel drowsy (sleepy) or dizzy.
    • They may get constipation (difficulty doing a poo).
    • Your child may feel sick (nausea) or be sick (vomit).
    • Your child may get headaches and sometimes feel dizzy due to low blood pressure.
    • Some children become agitated or restlessness at night.

    These side-effects usually wear off as your child’s body gets used to the medicine. If they continue after a week or so, or are a problem, contact your doctor.

    There may, sometimes, be other side-effects that are not listed above. If you notice anything unusual and are concerned, contact your doctor. You can report any suspected side-effects to a UK safety scheme at

    Can other medicines be given at the same time?

    • You can give your child medicines that contain paracetamol or ibuprofen, unless your doctor has told you not to.
    • Clonidine should not be taken with some medicines that you get on prescription. Tell your doctor and pharmacist about any other medicines your child is taking before giving clonidine.
    • Check with your doctor or pharmacist before giving any other medicines to your child. This includes herbal or complementary medicines.

    Is there anything else I need to know about this medicine?

    Do not stop giving clonidine to your child suddenly, as their blood pressure may become dangerously high.

    • If you or your child wants to stop this medicine, discuss this with your doctor. They will explain how to reduce the dose bit by bit. Do not reduce the dose without discussing this with your doctor.
    • Clonidine is also used to treat a range of other conditions, such as high blood pressure and pain.

    General advice about medicines

    • Try to give medicines at about the same times each day, to help you remember.
    • Only give this medicine to your child. Never give it to anyone else, even if their condition appears to be the same, as this could do harm.

    If you think someone else may have taken the medicine by accident, contact your doctor straight away.

    • Make sure that you always have enough medicine. Order a new prescription at least 2 weeks before you will run out. Specially ordered liquid medicine can take longer.
    • Make sure that the medicine you have at home has not reached the ‘best before’ or ‘use by’ date on the packaging. Give old medicines to your pharmacist to dispose of.

    Where should I keep this medicine?

    • Keep the medicine in a cupboard, away from heat and direct sunlight. It does not need to be kept in the fridge.
    • Make sure that children cannot see or reach the medicine.
    • Keep the medicine in the container it came in.

    Who to contact for more information

    Your doctor, pharmacist or nurse will be able to give you more information about clonidine and about other medicines used to treat Tourette’s syndrome, ADHD and sleep-onset disorder.

    About the author

    Leave a Reply

    Your email address will not be published. Required fields are marked *