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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

11 coronary patients, 8 with mild hypertension, were treated with clonidine, at a dose of 75 micrograms b.i.d. per os for a week. The effect of the drug on coronary heart disease was assessed by means of a symptom-limited multistage exercise test on the cycloergometer. Clonidine was effective in reducing the exercise-induced increases in blood pressure (by 15.5 +/- 6.1%), the double product (by 34.8 +/- 20.8%) and the electrocardiographic ischemic changes. In 2/4 patients, effort related ventricular extrasystoles were reduced by greater than 50% after clonidine. The drug worsened the anginal pain in 3 and relieved the pain in 3 patients. However, it reduced the exercise-induced ST-T segment downsloping in 7 patients. The tolerance was good, since only 3/11 patients reported slight dry mouth, sedation and pyrosis. In view of the electrocardiographic effect, further studies with clonidine on myocardial ischemia should be performed.
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PMID:The therapeutic value of clonidine in patients with coronary heart disease. 49 82

Clonidine is believed to reduce blood pressure by a neural action and animal experiments suggest that this consists in potentiation of baroreflexes. In 16 patients with essential hypertension we studied the effects of alterations in carotid sinus baroreceptor activity (neck chamber technique) on arterial blood pressure (catheter measurements) and heart rate, before and after intravenous administration of 150 microgram and 300 microgram of clonidine. The magnitude of the reflex responses was assessed by the slope of the linear regressions relating applied increase and decrease in tissue pressure at the carotid sinus (and therefore applied decrease and increase in carotid sinus transmural pressure) and resulting changes in mean arterial pressure and R-R interval. Clonidine caused a marked reduction in mean arterial pressure (-26 +/- 3 mm Hg) and a slight but significant reduction in heart rate (-5 +/- 1 b/min). There was no evidence for a potentiation of the baroreceptor influence on blood pressure, although a slight potentiation of the baroreceptor influence on heart rate was observed in few instances. We conclude that in man clonidine can exert a pronounced hypotensive effect without potentiating baroreceptor influence on blood pressure. Therefore this mechanism does not play a prominent role in the clinical antihypertensive action of the drug.
Hypertension
PMID:Clonidine and carotid baroreflex in essential hypertension. 54 Oct 39

The mechanism by which clonidine suppresses renin secretion was investigated in pentobarbital-anesthetized dogs in which renal perfusion pressure was controlled by means of an aortic clamp. Clonidine (30 microgram/kg, iv) lowered mean arterial pressure (MAP) from 124 +/- 8 to 104 +/- 4 mm Hg (P less than 0.01) and reduced plasma renin activity (PRA) to 32 +/- 4 percent of the control value (P less than 0.01) after 60 minutes. Ganglion blockade with pentolinium (3 mg/kg, im) decreased MAP from 148+/- 7 to 117 +/- 3 mm Hg (P less than 0.01) and reduced PRA to 55 +/- 13 percent of the control value (P less than 0.05) after 45 minutes. Pentolinium converted the hypotension produced by clonidine to hypertension (108 +/- 9 to 146 +/- 10 mm Hg at 60 minutes, P less than 0.05) and abolished the suppression of PRA (105 +/- 14 percent of control at 60 minutes, P less than 0.05). In a further series of experiments, the effects of oxymetazoline, an alpha-adrenergic receptor agonist which is closely related to clonidine but which does not cross the blood brain barrier, were studied. Oxymetazoline (10 microgram/kg, iv) increased MAP from 127 +/- 3 to 154 +/- 2 mm Hg (P less than 0.01) and elevated PRA TO 176 +/- 22 percent of the control value (P less than 0.02) after 30 minutes. A higher dose of oxymetazoline (30 microgram/kg) increased MAP from 129 +/- 10 to 161 +/- 9 mm Hg (P less than 0.05) and increased PRA to 256+/- 37 percent of control (P less than 0.05) after 30 minutes. Taken together, these data support the hypothesis that the inhibition of renin secretion by clonidine results from a centrally mediated decrease in sympathetic neural activity.
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PMID:Mechanism of suppression of renin secretion by clonidine in the dog. 62 Apr 41

Nineteen patients with severe essential hypertension or hypertension due to renal parenchymal disease were treated with intravenous clonidine. In 14 patients the elevated blood pressure was complicated by one or more crises: left ventricular failure in seven patients, encephalopathy in six, and subarachnoid hemorrhage, cerebral hemorrhage, dissecting aortic aneurysm, acute renal failure, and severe epistaxis, one episode each. Clonidine 0.15 or 0.30 mg, was given intravenously every 40 minutes until the diastolic blood pressure was decreased to 120 mm Hg or below. Blood pressure was taken every 10 minutes. Both systolic and diastolic blood pressure were reduced significantly after intravenous clonidine, the former by 96 mm Hg (P less than 0.001), the latter by 52 mm Hg (P less than 0.001) within a period of 40 minutes to 2 1/2 hours. The clonidine dose varied from 0.15 to 0.90 mg, mean 0.52 mg. Heart rate was decreased significantly by 20 beats/minute (P less than 0.001) by the drug. Serious side effects were not observed except for an episode of transient sinoatrial block. Renal function was not affected. Patients who were on chronic diuretic therapy prior to treatment with intravenous clonidine showed a significantly greater decrease in both systolic (P less than 0.01) and diastolic (P less than 0.001) blood pressure after the first clonidine dose. In one patient intravenous clonidine was not effective (i.e., blood pressure remained 200/150 mm Hg) in spite of a total clonidine dose of 0.9 mg. Two patients died, one from severe cerebral hemorrhage, the other from an extensive dissecting aortic aneurysm, but the fatal outcome was not related to clonidine.
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PMID:Evaluation of intravenous clonidine in hypertensive emergencies. 63 67

In order to determine the efficacy and safety of oral clonidine loading to control hypertension rapidly, 15 patients received 0.1 or 0.2 mg clonidine initially followed by hourly doses of 0.1 mg until the blood pressure was substantially reduced or until a total of 0.5 mg had been given. Twelve (80%) responded with a reduction in mean blood pressure of 33 +/- 3 (SE) mm Hg in an average time of 2.25 hr. Side effects were minimal. Four of the 5 patients hospitalized solely for purposes of blood pressure control responded to clonidine loading and were discharged the next day. Clonidine loading proved to be safe and effective for rapid control of hypertension and may be preferred to intravenous antihypertensives for some indications.
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PMID:Oral clonidine loading for rapid control of hypertension. 65 13

Clonidine (0.075-0.225 mg/day) and chlorthalidone (0.15-0.45 mg/day) were associated in the management of 23 cases of arterial hypertension of varying nature and gravity. A significant and satisfactory decrease in pressure was accompanied by reduced cardiac frequency. Diuresis, body weight and the main biohumoral indices were not significantly affected. The mechanism of action of the two drugs is explained and the reason why success was obtained with their combination in less-than-normal doses is discussed.
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PMID:[Clinical effects of a clonidine-chlorthalidone combination in the treatment of arterial hypertension]. 95 Oct 49

Clonidine hydrochloride is a new antihypertensive agent with a primary site of action in the central nervous system. When administered with a diuretic, it is effective for long-term therapy and may be particularly useful in patients with moderately severe hypertension. Clonidine is comparable to methyldopa in efficacy but may cause side-effects more frequently. The only potentially serious adverse reaction that has been reported is a rebound increase in blood pressure that may occur following rapid withdrawal.
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PMID:Evaluation of clonidine hydrochloride (Catapres). A new antihypertensive agent. 117 48

Effect of endothelin (ET) on clonidine induced cardiovascular effects was studied in male Sprague-Dawley rats. Clonidine (75 micrograms/kg, iv) produced significant decrease in blood pressure and heart rate. ET-1 (50 ng/kg, iv) pretreatment completely antagonized the hypotension and bradycardia induced by clonidine. ET-2 (50 ng/kg, iv) and ET-3 (50 ng/kg, iv) had similar antagonistic effect on clonidine induced hypotension and bradycardia. The antagonistic effect of ET lasted for several hours, however, 4 hours after ET pretreatment only partial blockade of clonidine induced hypotension and bradycardia was observed. This indicated that the antagonistic effect of ET was reversible. Initial hypertensive response induced by high dose of clonidine (750 micrograms/kg, iv) could not be antagonized by ET-1, ET-2 or ET-3, while phenoxybenzamine, an alpha adrenoceptor antagonist, blocked the hypertensive response of clonidine. Thus, ET has no antagonistic effect on the initial hypertensive response but antagonizes the hypotensive and bradycardic effect induced by clonidine. Clonidine induced hypotension and bradycardia are mediated through central alpha 2 adrenoceptors while hypertension is mediated through peripheral alpha 2 adrenoceptors. It is concluded that central alpha 2 adrenoceptors are different from peripheral alpha 2 adrenoceptors and ET antagonizes the effect of clonidine only on central alpha 2 adrenoceptors but has no antagonistic activity on peripheral alpha 2 adrenoceptors.
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PMID:Evidence for antagonistic activity of endothelin for clonidine induced hypotension and bradycardia. 130 33

Research on antihypertensive drugs not only provides new information on presently used agents but also leads to the introduction of exciting new compounds. Several important clinical trials involving currently available drugs have been published recently. Angiotensin-converting enzyme inhibitors improved survival in patients with milder degrees of congestive heart failure, which indicates that they have become the cornerstone of treatment for this condition. Angiotensin-converting enzyme inhibitors delayed or prevented the development of diabetic proteinuria (> 200 micrograms/min) in a placebo-controlled randomized trial. Further, enalapril was more effective than metoprolol in reducing the rate of decline in renal function in patients with type I diabetes. Calcium channel blockers protected against acute renal failure in patients after renal transplantation in two separate studies. Calcium channel blockers were shown to promote natriuresis, with negative sodium balance the same as that associated with thiazide diuretics. The voltage-dependent calcium channel has been cloned, and the binding sites of the three classes of calcium channel blockers are now known. beta-Blockers and thiazide diuretics were the drug treatments in the Systolic Hypertension in the Elderly Program trial and in the Swedish Trial in Old Patients with Hypertension study (patients 65 to 85 years). In both investigations, stroke and cardiovascular events were significantly reduced by these conventional inexpensive agents. Clonidine was found to lower blood pressure primarily by its interaction with the imidazole receptor rather than the alpha 2 receptor. Elucidation of the imidazole receptor promises to shed light on physiologic mechanisms as well as lead to the introduction of new agents, such as moxonidine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New classes of antihypertensive drugs and new findings with established agents. 136 36

Clonidine, idazoxan, rilmenidine, and comparable agents bind to imidazol(in)e (IR), as well as alpha 2-adrenergic, receptors. Interaction with IRs mediates the hypotension elicited by these drugs at their site of action in the rostral ventrolateral medulla oblongata (RVL) and probably the neuroprotection in focal ischemic cerebral infarction. Unlike alpha 2-adrenergic receptors, IRs are not coupled to G-proteins. Their native ligand may be clonidine-displacing substance (CDS), a potent, partially purified adrenomedullary secretagogue, distributed regionally in brain and some peripheral organs. IRs and CDS may be important in the genesis, expression, and/or therapy of hypertension and stroke.
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PMID:Imidazole receptors and clonidine-displacing substance in relationship to control of blood pressure, neuroprotection, and adrenomedullary secretion. 159 95


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