arAdrenergic Blockade and Cardiovascular Pressor Responses in Essential Hypertension

The effects of selective a,-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 a,-mediated, noradrenergic-dependent vasoconstriction. a,-Adrenergic receptor antagonism did not modify body sodium concentration, the adrenomedullary component of the sympathetic nervous system, angiotensin II levels, or /3-adrenergic dependent mechanisms. (Hypertension 8: 407-414, 1986)