Peripheral adrenergic receptors in hypertension.

Abstract

Increased sympathoadrenal activity appears to play an important role in the development or maintenance of elevated blood pressure in hypertensive patients and various annual models of hypertension. Alterations of adrenergic receptor number or responsiveness might contribute to this increased activity. We therefore reviewed the data on adrenergic receptor alterations in hypertension with special emphasis on several key cardiovascular tissues (i.e., heart, vascular smooth muscle, and kidney) and on lymphocytes and platelets as human tissues available for such studies. The data suggest that the number of o-adrenergic receptors in hypertension is regulated by catecholamines, dietary salt intake, and genetic factors. Increases in renal cv-adrenergic receptor number may be etiologic in genetic forms of essential hypertension. ^Adrenergic receptor alterations in states of elevated blood pressure do not appear to be specific for genetic hypertension. Desensitization of ^-adrenergic receptor function in hyper-tensive animals and patients contrasts with reports of decreased, unchanged, and increased /3-adrenergic receptor number, suggesting that signal transduction of /3-adrenergic (and possibly other) receptors that stimulate adenylyl cyclase is disturbed in hypertension. The mechanisms of such heterologous desensitization in states of elevated blood pressure remain to be elucidated. (Hypertension 1990;16:107-120)

Psychological States and Lymphocyte β-Adrenergic Receptor Responsiveness

“…Although we cannot rule out "white coat hypertension," our patients classified as "hypertensive" were so labeled only after repeated blood pressure measurement. Michel et al (1990) reported that the difference in ␤ -adrenergic receptor measures between hypertensives and normotensives is not consistent in many studies. We wanted to include as many subjects in our study as possible and compared ␤ -adrenergic receptor variables of hypertensive subjects with those of normotensive subjects.…”

β 2 -Adrenergic Receptor Gene Delivery to the Endothelium Corrects Impaired Adrenergic Vasorelaxation in Hypertension

“…Indeed, in hypertensive conditions, several reports indicate a reduction in ␤AR signaling and regulation. [5][6][7][8][9][10] If these premises hold true, improving ␤AR signaling should result in the restoration of ␤AR vasorelaxation. In fact, some interventions have been effective in correcting ␤AR signaling in hypertension, such as dietary salt restriction 7 or pharmacological treatment.…”

Variability in vascular responsiveness between Mexican–Americans and White Americans

“…Hyper-responsiveness of vascular smooth muscle to ␣ 1 -and ␣ 2 -adrenoceptor mediated vasoconstriction has been proposed as a factor in maintaining this increased resistance. 19 It is possible that hypo-responsiveness may play a protective role. Other investigators have found that vascular responsiveness to ␣ 1 -adrenergic stimulation with noradrenaline and phenylephrine is enhanced during the development of hypertension.…”