α1‐Adrenergic Blockade and Cardiovascular Pressor Responses in Essential Hypertension
作者:
CARLO BERETTA-PICCOLI,
CLAUDIA FERRIER,
PETER WEIDMANN,
期刊:
Hypertension
(OVID Available online 1986)
卷期:
Volume 8,
issue 5
页码: 407-414
ISSN:0194-911X
年代: 1986
出版商: OVID
关键词: terazosin;essential hypertension;α1-adrenergic receptors;norepinephrine;cardiovascular pressor responsiveness;body sodium;plasma renin activity;aldosterone;cardiac β-adrenergic receptor response
数据来源: OVID
摘要:
The effects of selective α1-adrenergic blockade with terazosin on blood pressure and cardiovascular pressor responsiveness were assessed in 17 subjects with mild to moderate essential hypertension (mean age, 48 ± 2 [SEM] years). As compared with a 2-week placebo period, 8 weeks of terazosin treatment (mean dose, 10.5 ± 1.7 mg/day) caused a fall of supine (from 153/103 ± 3/2 to 143/96 ± 4/2 mm Hg;p< 0.025) and upright (from 145/106 ± 4/2 to 131/94 ± 5/3 mm Hg;p< 0.01) arterial pressure; a marked blunting of cardiovascular pressor responsiveness to norepinephrine, as judged from the pressor dose (from 73 ± 9 to 2156 ± 496 ng/kg/min;p< 0.02) and from the rightward shift (p< 0.01) of the plasma concentration-blood pressure response curve; and a slight increase in plasma norepinephrine concentration (from 37.7 ± 3.3 to 52.2 ± 7.8 ng/dl;p< 0.01). Heart rate, body weight, exchangeable sodium, blood volume, and norepinephrine plasma clearance; plasma epinephrine, renin, angiotensin II, and aldosterone levels; the relationships between angiotensin H-induced increases in arterial pressure or plasma aldosterone and the concomitant increments of plasma angiotensin II; and heart rate responsiveness to isoproterenol did not change significantly after terazosin treatment. These findings suggest that the fall of arterial pressure induced by selective,-adrenergic blockade in subjects with essential hypertension is associated with, and probably explained by, inhibition of α1-mediated, noradrenergic-dependent vasoconstriction. α1-Adrenergic receptor antagonism did not modify body sodium concentration, the adrenomedullary component of the sympathetic nervous system, angiotensin II levels, or β-adrenergic dependent mechanisms.
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