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

Diurnal rhythm of plasma beta endorphin was established with the highest level in the morning and the lowest one at midnight in normotensive subjects and also in patients with essential hypertension. Clonidine (300 micrograms daily) significantly increased plasma beta endorphin concentrations only in the hypertensive patients. The significant linear correlation between the increase in plasma beta endorphin concentration and the decrease in blood pressure (both systolic and diastolic) in these patients may point to the role of this endogenous opioid in the antihypertensive action of clonidine.
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PMID:Diurnal rhythm of beta endorphin in normotensive and hypertensive patients: the effect of clonidine. 630 Jan 70

Reports on spontaneously hypertensive rats suggested that naloxone blocked the antihypertensive effects of clonidine. We compared the effects of an 8-hr intravenous naloxone infusion (6 micrograms/kg/hr) or 5% dextrose in water (D5/W) begun 2 hr before single oral doses of clonidine (0.3 mg) in six men with mild to moderate essential hypertension (EHT). Supine and standing (after 5 min) blood pressure (BP) and heart rate (HR) were measured every 20 min. Initial treatment with naloxone or placebo (D5/W) infusion was randomly allocated, with the alternate treatment given 1 wk later. Naloxone did not modify either supine or standing BP or HR. Clonidine induced a gradual, sustained reduction in both supine and standing systolic and diastolic BP and in supine HR, and there was an increase in standing HR. Naloxone did not modify the onset, maximal effect, or recovery of the hypotensive and HR effects of clonidine in both the supine and standing positions. Our data indicate that hypotensive and bradycardiac effects of clonidine in EHT are not mediated by naloxone-sensitive opioid receptors. They also suggest that opioid receptors play no role in the maintenance of hypertension nor in the BP and HR adjustments induced by postural changes in EHT.
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PMID:Naloxone does not antagonize the antihypertensive effect of clonidine in essential hypertension. 630 46

Studies in animals and man indicate a functional interaction between the adrenergic and the opiate systems. In the present study the effect of the opiate receptor blocker naloxone on the increase in plasma GH induced by clonidine was investigated in eight patients with essential hypertension. In a randomized order the patients received a bolus dose of naloxone (10 micrograms/kg) or physiological saline followed by a slow infusion of naloxone (5 micrograms/kg X h) or saline, respectively. Fifteen minutes after the bolus dose of saline or naloxone, clonidine (3 micrograms/kg) was infused for 10 min. Clonidine induced a significant increase in plasma GH. Naloxone pretreatment resulted in a significantly reduced GH increase after the clonidine infusion. These results indicate that the clonidine-induced increase in plasma GH in hypertensive man is partly mediated via activation of opiate receptors which can be blocked by naloxone.
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PMID:Partial blockade by naloxone of clonidine-induced increase in plasma growth hormone in hypertensive patients. 631 49

These studies were undertaken to clarify the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension (EH), and the following examinations were performed: 1) Urinary free norepinephrine and epinephrine excretion (UNEf and UEf), urinary conjugated norepinephrine and epinephrine excretion (UNEconj and UEconj), plasma norepinephrine and epinephrine concentration (PNE and PE), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) were measured in 52 patients with EH, who were divided into two groups (borderline EH: b-EH, and sustained EH: s-EH), and fifteen normals (N). 2) Cardiac index (CI), total peripheral resistance index (TPRI), appearance time, mean transit time and stroke index (SI) were determined by the dye-dilution method in eight patients with b-EH, ten patients with s-EH and ten N. 3) Clonidine was administered orally in a single dose of 150 micrograms to seven patients with s-EH and three patients with b-EH, and PNE, PE and growth hormone (GH) were measured before and after the administration. 4) Isoproterenol was infused intravenously in a dose of 0.02 microgram/kg/min for 30 min to 18 patients with s-EH and six N, then plasma cyclic AMP (c-AMP) and PRA were determined before, during and after the infusion. 5) Methacholine was injected intramuscularly in a dose of 10 mg to seven N, and PNE, PE and PRA were measured before and after the injection. There were no significant differences of PNE, PE, UNEf and UEf among the three groups (b-EH, s-EH and N), but UNEconj in both b-EH and s-EH was higher than in N (b-EH: p less than 0.1, s-EH: p less than 0.05). PRA in s-EH was slightly lower not only in N but also in b-EH. PAC in b-EH and s-EH was slightly lower than in N. The difference of PAC between b-EH and s-EH was not found. CI and SI were higher than in N (p less than 0.05), but TPRI was normal. In s-EH, TPRI was slightly elevated as compared with b-EH (p less than 0.1). In s-EH, clonidine caused a significant lowering of both blood pressure and PNE with a simultaneously marked increment of GH; on the other hand, in b-EH blood pressure and PNE did not change significantly in spite of the distinct rise of GH. After the isoproterenol infusion, PRA and c-AMP increased, and there was a significant correlation between the initial level of PRA and the maximal increment of PRA after the infusion in both s-EH and N.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Studies on the role of the central and peripheral sympathetic nervous system and the renin-aldosterone system on the onset and maintenance of high blood pressure in essential hypertension]. 632 58

Fifteen patients with essential hypertension and ten with pheochromocytoma were studied to assess the effect of clonidine, a centrally acting antihypertensive agent, on the functional and biochemical indices of sympathetic function. Single oral doses of clonidine (0.3 mg) decreased supine plasma norepinephrine significantly in essential hypertension, but not in pheochromocytoma despite producing similar reductions in blood pressure and heart rate. Plasma renin activity was unchanged in both groups. In untreated essential hypertension, head-up tilt increased diastolic blood pressure, heart rate, and plasma norepinephrine. Three hours after a single oral dose of clonidine, head-up tilt resulted in significant blood pressure reductions, although heart rate and plasma norepinephrine increased dramatically. Clonidine might reduce blood pressure by inhibiting sympathetic outflow, and any effect on plasma renin activity appears unimportant in its antihypertensive action. In pheochromocytoma clonidine decreases blood pressure without altering plasma norepinephrine, which is consistent with the concept that the norepinephrine released from axon terminals of sympathetic postganglionic neurons is biologically more significant than circulating catecholamines.
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PMID:Effects of clonidine on sympathetic function. 633 29

Clonidine was given to patients with essential hypertension, renovascular hypertension, and hypertension with parenchymal renal disease. The drug was effective in all groups but was more effective in patients with high plasma renin concentration. Renal function did not deteriorate when the drug was used, and there was an increase in renal blood flow and a small increase in glomerular filtration rate in those with renovascular or essential hypertension. These changes may have been due to falls in plasma renin. Clonidine can be used in patients with renal disease and does not cause worsening of renal function.
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PMID:The use of centrally acting antihypertensive drugs in patients with renal disease. 633 30

Antihypertensive medications have a variable effect on renal hemodynamics and may contribute to renal insufficiency in some patients. Since clonidine has actually been found to improve renal hemodynamics in patients with essential hypertension, we studied the effects of clonidine therapy in patients with renal transplant hypertension. Baseline measurements of BP and renal hemodynamics were made in six patients after two weeks of therapy with furosemide. Clonidine was then added and titrated until BP was controlled. Repeated measurements of renal hemodynamics were made four and 16 weeks after clonidine therapy was begun. Glomerular filtration and effective renal plasma flow as assessed by inulin and aminohippurate sodium clearances were preserved during prolonged clonidine therapy.
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PMID:Effect of clonidine therapy on renal hemodynamics in renal transplant hypertension. 637 12

The acute and chronic effects of fixed dosages of clonidine and prazosin on supine and upright blood pressure, the renin-angiotensin-aldosterone system, and plasma catecholamines were compared in 24 patients with essential hypertension. The patients were randomized into two groups; 11 received chlorthalidone (50 mg daily) throughout the protocol, but 13 received no diuretic. Clonidine was generally more effective in lowering systolic and diastolic blood pressure in the supine posture throughout the study; prazosin tended to decrease blood pressure in the upright posture more effectively, especially during the first week of treatment. The only truly significant difference was found after four weeks of treatment when the decrease in supine systolic blood pressure by clonidine of 26.5 +/- 8.9 mm Hg was greater than that of 1.7 +/- 5.6 mm Hg produced by prazosin (P less than .05).
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PMID:Comparative antihypertensive and endocrinologic effects of clonidine and prazosin in patients with essential hypertension. 638 78

Daily doses of 0.3 mg clonidine and 3 mg guanfacine were equiactive in decreasing blood pressure and heart rate in 17 subjects with essential hypertension. Clonidine decreased cardiac output and guanfacine decreased total peripheral resistance, while clonidine had no effect on stroke volume but guanfacine increased it. Both clonidine and guanfacine decreased plasma renin activity. Naloxone, 0.4 mg iv, reversed the antihypertensive effect of clonidine but was ineffective even at higher doses (1.6 mg iv) when subjects were treated with placebo or guanfacine. It is suggested that the hemodynamic differences between the two centrally acting alpha 2-adrenoceptor agonist antihypertensive drugs may at least in part result from the involvement of opioid mechanisms only in the action of clonidine.
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PMID:Effects of clonidine and guanfacine in essential hypertension. 638 75

Cerebrospinal fluid (CSF) catecholamines were measured in normotensive patients and in patients with mild to moderate essential hypertension. CSF-norepinephrine (NE) concentrations were 50% lower in the normotensive individuals (127 +/- 28 vs. 240 +/- 23 pg/ml) (P less than 0.01). In hypertensive patients, CSF-NE was inversely related to age (r = -0.68; P less than 0.01) and directly related to plasma NE (r = 0.61; P less than 0.05). Clonidine (450 mcg/day for 2 weeks) significantly reduced CSF-NE (-40%) in hypertensive patients. In addition, it decreased blood pressure, plasma and urinary NE. Urinary VMA was not affected by clonidine. No correlation was observed between clonidine effects on BP and on plasma or CSF catecholamines. This study indicates that patients with essential hypertension have elevated levels of CSF-NE which are reduced after treatment with clonidine. The elevation of CSF-NE suggests that central (spinal?) noradrenergic activity may be increased in patients with mild to moderate essential hypertension, and that can be reduced by treatment with clonidine.
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PMID:Clonidine reduces elevated cerebrospinal fluid catecholamine levels in patients with essential hypertension. 648 58


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