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Query: UMLS:C0085580 (essential hypertension)
 14,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
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PMID:Clonidine and carotid baroreflex in essential hypertension. 54 Oct 39

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

Clonidine failed to reduce the blood pressures of two patients with essential hypertension. On was given 5-4 mg/day and the other 6 mg/day, and their respective peak plasma clonidine concentrations were 26-2 ng/ml and 14-4 ng/ml. Several months after the end of clonidine treatment a single oral dose of 0-3 mg of clonidine produced maximum falls in blood pressure of 30/22 mm Hg and 88/41 mm Hg with peak plasma clonidine concentrations of 1-4 ng/ml and 0-9 ng/ml. Resistance to the hypotensive effect of high doses of clonidine may be due to stimulation of peripheral alpha-adrenoceptors causing vasoconstriction, which maintains a raised blood pressure.
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PMID:Apparent resistance to hypotensive effect of clonidine. 83 37

Systolic time intervals, including preejection period (PEP) and left ventricular ejection time (LVET), were studied in patients with permanent essential hypertension before and after intra-venous administration of propranolol 0.2 mg/kg (11 patients), clonidine 0.002 mg/kg (10 patients) and methyldopa 2 mg/kg (12 patients). With propranolol, diastolic blood pressure was unchanged and the heart rate decreased, whilst PEP and LVET were significantly prolonged (P less than 0.001). Clonidine caused a fall in blood pressure (P less than 0.001), heart rate was slightly reduced, PEP was prolonged (P less than 0.001) and there was a significant decrease in LVET at 5 min. With methyldopa, no significant effect was observed after intravenous injection, but 7 days oral administration produced the identical effect as clonidine. These observations suggest that certain antihypertensive drugs may impair left ventricular performance and depress myocardial contractility.
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PMID:Effect of certain antiadrenergic agents on systolic time intervals in essential hypertension. 89 85

Clonidine, 225 mug a day, has been given orally for 3 months to 15 patients with essential hypertension. Mean BP was reduced from 159/107 to 143/87 mmHg. The antihypertensive effect of the drug was dissociated from changes in plasma renin activity (PRA) during clonidine treatment. PRA levels decreased initially in 6 patients with the highest PRA values before treatment, but then increased again. In 6 patients with lower pretreatment PRA levels, PRA rose continuously. Opposite patterns of 24-hour urinary sodium excretion were observed in these arbitrary subgroups. The antihypertensive effect of clonidine in essential hypertension appears to be independent of changes in PRA.
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PMID:Plasma renin activity, blood pressure and sodium excretion during treatment with clonidine. 115 20

The effects of the antihypertensive imidazoline compounds 2-(5 fluor-0-toluidine)-2-imidazoline hydrochloride (ST 600) and 2-(2, 6 dichlorophenylamine)-2-imidazoline hydrochloride (ST 155, clonidine, Catapres) on intra-arterial pressure, cardiac output, stroke volume, heart rate, total peripheral resistance, renal blood flow, glomerular filtration rate, renal vascular resistance, plasma volume, plasma renin and aldosterone concentration were studied in five patients with essential hypertension. The antihypertensive action of both compounds was similar and was accompanied by a reduction in heart rate and in cardiac output, total peripheral resistance being unchanged. There was no significant decrease in renal blood flow and glomerular filtration rate. Plasma volume and plasma concentrations of renin and aldosterone also did not change significantly. In the face of similar reductions in blood pressure, no differences were observed between cardio-renal haemodynamic responses after ST 600 and clonidine. However ST 600 had a longer lasting effect (8-12 hours).
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PMID:Comparison between the effects of ST 600 and clonidine. 119 Sep 9

In patients with primary hypertension, intravenous administration of 150 mug Clonidin caused a decrease in arterial pressure, renin activity, RPF, GFR and electrolyte excretion. Activation of intracerebral adrenergic alpha-receptors and diminished sympathetic outflow seem to be responsible for the decrease of renin release.
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PMID:[The effect of clonidine on renin-release (author's transl)]. 126 3

Short-term fluctuations in blood pressure (BP) and heart rate (HR) were analyzed in a group of eight men with essential hypertension. Indirect finger BP was measured by a Finapres device. Analog-to-digital conversion of the BP was used to determine systolic (SAP), diastolic (DAP), and mean arterial pressure (MAP) and HR every second. The equidistant sampling allowed a direct spectral analysis using a fast Fourier transform algorithm. The effects of an oral dose of clonidine (150 micrograms) were studied in a double-blind, crossover, placebo-controlled study. Clonidine markedly reduced the variability of BP and HR after 90 min as indicated by a reduction in the standard deviations of BP by 36.7% for SAP, 21.0% for DAP, 22.1% for MAP, and 26.0% for HR. At this time clonidine reduced the average BP by 19.7 mm Hg for SAP, 10.6 mm Hg for DAP, 16.0 mm Hg for MAP, and 1.0 beat/min for HR. Spectral profiles of BP and HR illustrated the alterations in the spontaneous oscillations underlying the standard deviation changes. Clonidine dramatically reduced the amplitude of BP and HR oscillations in the mid-frequency region 66-129 mHz, which depends on the activity of the autonomic nervous system. We suggest that an increased sensitivity of the baroreflex is responsible for the apparent better control of BP and HR with clonidine.
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PMID:Clonidine reduces blood pressure and heart rate oscillations in hypertensive patients. 171 18

Clonidine, an agonist of central alpha-2-adrenergic receptors, reduced the peripheral sympathetic activity. With regard to the mutual pathophysiological relationship of blood pressure regulating mechanisms, the authors wanted to find out whether after clonidine administration, in addition to the known suppression of catecholamine levels (CA), also changes in the concentration of other pressor and depressor humoral substances will occur. They investigated therefore in 15 patients with essential hypertension (EH) and in three patients with pheochromocytoma the urinary excretion of free noradrenaline (NA), adrenaline (A) and dopamine (DA), the plasma renin activity (PRA), the aldosterone concentration (PAC) and atrial natriuretic factor (ANF) in plasma, using radioimmunoanalysis, always before and 24 hours after clonidine administration (Haemiton retardR) by the oral route. Its administration led in patients with EH to a decline of NA and DA. On the other hand, in pheochromocytoma their urinary excretion did not change in an unequivocal way, and when it declined, never normal NA and DA levels were reached. A excretion remained unaltered in both groups of patients. The drop of PRA after clonidine as a result of the drop of peripheral adrenergic activity was not associated with an expected parallel drop of PAC but by its rise. This effect can be explained by a reduction of the tonic inhibition of PAC output when the DA level declines. The rise of ANF after clonidine administration will be the subject of subsequent investigations. It cannot be ruled out that this effect is due to the direct action of clonidine on alpha receptors in the heart.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The effect of clonidine on humoral factors in patients with arterial hypertension]. 214 Feb 96

The study objective was to determine the effects of monotherapy with clonidine and atenolol versus placebo on serum lipids, apolipoproteins, and blood pressure in patients with mild primary hypertension. The protocol comprised a double blind, randomized, placebo-controlled 5-month prospective study carried out in an outpatient general internal medicine clinic in a university medical center. There were 92 patients ages 18 to 70, with mild primary hypertension (sitting diastolic blood pressure of greater than 90 mm Hg and less than 105 mm Hg) without significant cardiac, renal, cerebrovascular, hepatic, neoplastic, or hematologic disorders. Patients with severe hyperlipidemia or peripheral vascular disease were also excluded. All factors known to effect serum lipids were held constant throughout the study (i.e., diet, weight, exercise, caffeine, tobacco). Atenolol and clonidine significantly reduced blood pressure when compared with placebo. Atenolol caused significant increases in serum triglycerides and apolipoprotein B (p less than 0.05) and significant reductions in high-density lipoprotein-cholesterol, apolipoproteins A-I and A-II (p less than 0.05). Atenolol also induced a significant adverse effect on all lipid ratios, increasing total cholesterol/high density lipoprotein-cholesterol, low density lipoprotein-cholesterol/high density lipoprotein-cholesterol, apolipoprotein B/apolipoprotein A-I and apolipoprotein B/apolipoprotein A-II ratios and decreasing low density lipoprotein-cholesterol/apolipoprotein-B ratio (p less than 0.05). Clonidine caused significant reductions in high-density lipoprotein-cholesterol, apolipoproteins AI and AII (p less than 0.05 but was neutral on all other lipids, lipid subfractions, and apolipoproteins. Clonidine did not significantly alter any of the lipid ratios.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of clonidine hydrochloride versus atenolol monotherapy on serum lipids, lipid subfractions, and apolipoproteins in mild hypertension. 219 93


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