Affiliation:
1. Department of Medicine, University of California, San Diego.
Abstract
Previous biochemical assessment of sympathetic nervous system activity including plasma catecholamines, plasma renin activity, and plasma dopamine-beta-hydroxylase levels has suggested racial differences in the contribution of the sympathetic nervous system to the pathogenesis or maintenance of hypertension. We, therefore, performed physiological and pharmacological studies in white and black subjects with essential hypertension and their age-matched normotensive counterparts to assess autonomic and sympathetic nervous system function. One hundred one male subjects (47 white hypertensive, 17 black hypertensive, 22 white normotensive, and 15 black normotensive subjects) were evaluated for baroreceptor reflex sensitivity to low-pressure (amyl nitrite inhalation) and high-pressure (phenylephrine infusion) stimuli; cold pressor test heart rate and blood pressure responses; and blood pressure response to phentolamine alpha-adrenergic blockade. Hypertensive subjects exhibited an increase in resting heart rate, a decrease in baroreceptor reflex sensitivity, and an exaggerated decline in mean arterial pressure in response to phentolamine. These abnormalities were present to a comparable degree in black and white hypertensive subjects. Cold pressor testing revealed greater increases in heart rate in blacks as compared with whites; however, this racial difference was present regardless of blood pressure status, occurring in black normotensive and black hypertensive subjects to a comparable degree. Cold pressor test blood pressure increments were similar in the four groups. We conclude that both white hypertensive and black hypertensive subjects demonstrate similar abnormalities in autonomic and sympathetic nervous system function including blunting of baroreceptor reflex sensitivity and an increased alpha-adrenergic receptor participation in blood pressure maintenance. The results do not suggest major racial differences in autonomic pathogenetic mechanisms in hypertension.
Publisher
Ovid Technologies (Wolters Kluwer Health)
Subject
Physiology (medical),Cardiology and Cardiovascular Medicine
Cited by
52 articles.
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