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

Several authors have discussed an alteration of adrenergic receptivity in arterial hypertension. De Champlain (Hypertension 1990; 8: S77-S85) suggested that postsynaptic alpha 1-adrenergic functions became dominant while beta-adrenergic functions are attenuated in arterial hypertension. However, the status of presynaptic alpha 2-adrenoceptors remains unknown. The present study investigates presynaptic alpha 2-adrenoceptors in hypertension through the measurement of plasma levels of noradrenaline after administration of yohimbine, an alpha 2-adrenoceptor antagonist, in essential hypertension. Yohimbine (0.2 mg/kg per os) induced a 73% increase of plasma levels of noradrenaline in hypertensive patients (n = 12) and a 178% one in normotensive subjects (n = 6, p < 0.05). A similar significant difference was found in experimental neurogenic hypertension observed in awake dogs 3 weeks after sinoaortic denervation: the increase in plasma concentrations of noradrenaline after yohimbine (0.5 mg/kg i.v.) was +279% in hypertensive versus +642% in normotensive dogs (p < 0.05). The results show that the magnitude of the yohimbine-induced sympathetic activation is lower in hypertensives than in normotensives. They suggest the existence of a presynaptic alpha 2-adrenoceptor desensitization in arterial hypertension. The abnormality of this presynaptic inhibitory mechanism can increase the sympathetic tone and help to develop and maintain arterial hypertension.
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PMID:[Is there any desensitization of presynaptic alpha 2-adrenergic receptors in hypertension? Experimental and clinical studies]. 136 44

Systemic administration of yohimbine augments sympathetic outflow and blocks presynaptic alpha 2-adrenergic receptors, releasing the sympathetic neurotransmitter norepinephrine (NE) into the bloodstream. The present study examined sympathoadrenal and hemodynamic responses to yohimbine in 19 patients with essential hypertension and 19 normotensive control subjects. Baseline mean values for arterial NE, epinephrine, dihydroxyphenylglycol (the main intraneuronal metabolite of NE), spillover of NE into arterial plasma, and corticotropin did not differ between the hypertensive and normotensive groups. Yohimbine (0.125 mg/kg i.v. bolus followed by 0.001 mg/kg/min infusion for a total of 15 minutes) increased mean arterial pressure in all but one subject (by 13 +/- 2% [SEM] in the normotensive and 17 +/- 2% in the hypertensive group) and increased arterial NE levels in all subjects (by 253 +/- 50 pg/ml in the normotensive and 312 +/- 51 pg/ml in the hypertensive group). Among hypertensive patients, pressor, cardiac, output, and arterial NE responses were distributed bimodally. Patients with large hemodynamic and NE responses to yohimbine typically reported a history of anxiety, depression, or other psychopathology and of marked pressor or tachycardic episodes during emotional stress. In the hypertensive and normotensive groups, baseline arterial NE concentrations predicted the magnitude of pressor responses to yohimbine (r = 0.59, r = 0.54,p less than 0.01), whereas baseline mean arterial pressure was unrelated to the pressor response. A yohimbine challenge test can identify patients with pressor hyperresponsiveness and can distinguish patients with pressor hyperresponsiveness due to excessive sympathoadrenal reactivity from patients with enhanced postsynaptic responsiveness to endogenous NE.
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PMID:Sympathetic reactivity during a yohimbine challenge test in essential hypertension. 165 75

The development of specific binding techniques for the study of adrenergic receptors on circulating human blood cells has allowed a better understanding of the physiological alterations of adrenergic receptors and changes of adrenergic receptors in pathological conditions such as hypertension. Alpha adrenoceptors play an important part in blood pressure regulation at several sites. There are contradictory and conflicting reports on whether alpha receptor mechanisms are altered in essential hypertension. To address further the role of alpha 2 adrenoceptors in human essential hypertension the number and the affinity of alpha 2 adrenergic receptors and plasma catecholamine levels were measured in 20 normotensive and 24 hypertensive subjects. The median number of receptors (Bmax) was 159.10 +/- 14.38 fmol/mg protein for controls versus 179.09 +/- 13.26 fmol/mg protein for hypertensives. The median dissociation constant (KD) of the receptors for 3H-Yohimbine was 1.43 +/- 0.17 nmol/l for controls and 1.85 +/- 0.19 nmol/l for hypertensives patients. There were no differences in catecholamine plasma levels between the two groups. In controls platelet alpha 2 receptor number correlated with age (p less than 0.003) but not with blood pressure values. Our results show that measurement of platelet alpha 2 receptor levels and affinity is unable to differentiate a group of hypertensives from normotensives. Nevertheless, we cannot exclude a possible role of peripheral alpha 2 adrenergic receptors in the pathogenesis of high blood pressure.
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PMID:[Regulation of platelet alpha2 adrenergic receptors in a population of patients with essential arterial hypertension and in normotensive subjects]. 166 51

To confirm the presence of alpha 2-mediated vasoconstriction in human vasculature, the effect of selective alpha 1- and alpha 2-agonists (methoxamine and B-HT 933) and antagonists (indoramin and Yohimbine) was studied in fourteen patients with mild, uncomplicated, essential hypertension. Drugs were infused, into the brachial artery at systemically ineffective rates, and concomitant changes in forearm blood flow were measured by strain gauge venous plethysmography. During control conditions, cumulative infusions either of methoxamine or B-HT 933 caused dose-related vasoconstriction, while both indoramin and yohimbine doubled forearm blood flow. Subsequently, the alpha 1-adrenoceptor mediated vasoconstriction produced by methoxamine was shown to be completely blocked by indoramin pretreatment, and to be left unchanged by yohimbine. The alpha 2-vascular stimulation by B-HT 933 was antagonized by previous yohimbine but not by indoramin pretreatment, thus fulfilling the pharmacological requirements for identification of distinct alpha-adrenoceptor mediated excitation-contraction pathways. The data provide further evidence of the existence of alpha 2-mediated vasoconstriction in human forearm vessels.
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PMID:Further evidence for the existence of alpha 2-mediated adrenergic vasoconstriction in human vessels. 284 Nov 37

Since it is not known for certain which alpha-adrenergic receptors mediate renal vasoconstriction in human essential hypertension, we infused either doxazosin (n = 7) or yohimbine (n = 7) into the renal arteries of hypertensive subjects immediately prior to diagnostic angiography. Both agents caused an increment in renal blood flow as assessed with the xenon-washout technique. Doxazosin increased renal flow from 342 +/- 36 to 360 +/- 55 ml/min per 100 g (0.05 less than p less than 0.10). Yohimbine enhanced flow from 380 +/- 41 to 485 +/- 63 ml/min per 100 g (p less than 0.01). The effect of yohimbine was significantly greater than that of doxazosin. In a control group (n = 7) receiving only saline, no changes in renal blood flow occurred. Doxazosin enhanced renin secretion in the kidney by 10 +/- 4% over levels in controls (0.05 less than p less than 0.10), whereas yohimbine increased renin release by 80 +/- 23% (p less than 0.01). The latter increase was apparently not due to alterations in flow alone, since the arteriovenous gradient for renin also widened. We conclude that in resting conditions, neurogenic vascular tone in the kidney depends mainly upon activation of alpha 2-adrenergic receptors. Moreover, these receptors exert a tonic inhibitory influence on renin release.
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PMID:Role of alpha 1- and alpha 2-adrenergic receptors in the human hypertensive kidney. 288 75

Alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction were compared between 13 patients with essential hypertension and 13 normotensive controls, matched for age and sex. For this purpose changes in forearm blood flow induced by infusion of the selective alpha 1-adrenoceptor agonist methoxamine, the selective alpha 2-adrenoceptor agonist B-HT 933, the catecholamines adrenaline and noradrenaline and the alpha 2-adrenoceptor antagonist yohimbine were measured in both study groups. The catecholamines were infused together with propranolol to avoid beta-adrenergic effects. Forearm blood flow was measured by plethysmography. All agonists produced a dose-dependent vasoconstriction which was more pronounced in the hypertensive subjects but no preference was found for either the alpha 1- or alpha 2-adrenoceptor mediated vasoconstriction. Yohimbine induced a greater vasodilatation in the normotensive subjects. The greater vasoconstriction in the hypertensive patients could be explained by structural vascular changes. No evidence was found for an important role of alpha 2-adrenoceptor mediated vasoconstriction in essential hypertension.
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PMID:Alpha 1- and alpha 2-adrenoceptor mediated vasoconstriction in the forearm: differences between normotensive and hypertensive subjects. 290 22

The purpose of this study has been to test the hypothesis of an alpha 2-adrenoreceptor alteration in human essential hypertension. The design of the study involved the oral administration of 10 mg yohimbine, an alpha 2-adrenergic antagonist, to 25 healthy volunteers and 29 sex- and age-matched untreated hypertensive patients. Volunteers and patients were studied twice in random order, after placebo or yohimbine treatment, in supine and upright positions. Arterial pressure and heart rate were monitored by servoplethysmomanometry, and venous plasma catecholamines were determined by HPLC with electrochemical detection. Yohimbine induced a significant increase in diastolic pressure only in the hypertensive patients. Plasma norepinephrine was increased significantly in both yohimbine-treated groups, but the percent increase of plasma norepinephrine after the standing test was decreased significantly only in the healthy yohimbine-treated subjects. Plasma dopamine was increased significantly only in the healthy yohimbine-treated subjects. The response of plasma dopamine to the upright position was modified only in the healthy yohimbine-treated subjects. The decrease observed after 2 min of standing was abolished, showing the involvement of alpha 2-adrenoreceptors in the physiologic response of plasma catecholamines in healthy volunteers. Our data may be consistent with some in vivo evidence of an alpha 2-adrenoreceptor desensitization or an alteration in the balance of alpha-adrenoreceptors in human hypertension.
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PMID:Yohimbine effects on blood pressure and plasma catecholamines in human hypertension. 766 40

Yohimbine is an alpha 2-adrenoceptor antagonist that is FDA approved for treatment of impotence. The drug is an indolalkylamine alkaloid chemically similar to reserpine and is believed to act through sympatholysis. We examined effects of oral yohimbine on blood pressure (BP) and plasma levels of catechols in patients with essential hypertension, a condition in which most drug treatments can produce impotence. In 25 unmedicated hypertensive subjects, vital signs were measured and blood samples were obtained through an indwelling antecubital venous catheter at baseline and 1 and 2 h after subjects ingested 4 5.4-mg tablets of yohimbine. Mean blood pressure (MBP) increased by an average of 5 mm Hg (p < 0.01), plasma norepinephrine (NE) levels increased by 66% (p < 0.001), and plasma dihydroxyphenylglycol (DHPG) levels increased by 25% (p < 0.01) at 1 h after drug administration. The magnitude of the pressor response was unrelated to baseline MBP but positively correlated with the baseline NE level (r = 0.61, p < 0.01) and with the yohimbine-induced increment in plasma NE (r = 0.4, p < 0.01). The results indicate that yohimbine does not inhibit and actually stimulates sympathetically mediated NE release in humans and that the increased NE release produces a pressor response. Yohimbine should be administered with caution to patients with high BP, especially in individuals with evidence for increased basal sympathetic outflow or those undergoing concurrent treatment with tricyclic antidepressants or other drugs that interfere with neuronal uptake or metabolism of NE.
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PMID:Oral yohimbine increases blood pressure and sympathetic nervous outflow in hypertensive patients. 769 91

We have studied the sympathetic response to blockade of presynaptic alpha 2-adrenoceptors in essential hypertension by measuring plasma concentrations of noradrenaline after a single oral dose of yohimbine, an alpha 2-adrenoceptor antagonist. Mean baseline plasma noradrenaline and adrenaline concentrations were similar in the hypertensive and normotensive groups. Yohimbine (0.2 mg x kg-1 orally) caused a lesser increase in the plasma concentrations of noradrenaline in hypertensive patients (+67%) than in normotensive subjects (+178%) and a pressor response in hypertensive (but not in normotensive) patients. These results are consistent with an alteration in the balance of alpha-adrenoceptors (for example presynaptic alpha 2-adrenoceptor desensitization and post-synaptic alpha 1-adrenoceptor hyper-responsiveness) which would help to develop and/or maintain arterial hypertension.
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PMID:The effect of yohimbine on sympathetic responsiveness in essential hypertension. 845 67