Captopril modifies the hemodynamic and neuroendocrine responses to sodium nitroprusside in hypertensive patients.

Abstract

SUMMARY To determine if clinically effective doses of the antihypertensive agent captopril affected the neuronal release of norepinephrine or baroreflex sensitivity, changes in plasma norepinephrine concentration and heart rate were related to the changes in mean arterial pressure seen during the intravenous infusion of stepwise incremental doses of sodium nitroprusside before and during captopril treatment in eight hypertensive men with normal or low plasma renin activity. At all times, significant linear correlations were found between 1) the decrease in mean arterial pressure and the dose of sodium nitroprusside, 2) the increase in heart rate and the decrease in mean arterial pressure, and 3) the increase in plasma norepinephrine concentration and the decrease in mean arterial pressure. When the subjects were treated with captopril (25 mg t.i.d.) for 2 to 4 weeks, supine mean arterial pressure decreased from 130 to 114 mm Hg (-12%; p < 0.05), heart rate did not change, supine and upright plasma renin activity increased, while supine plasma norepinephrine and epinephrine concentration decreased slightly. Therapy with captopril (25 mg t.i.d.) increased baroreflex sensitivity, as assessed by the slope of the regression line relating the increase in heart rate to the decrease in mean arterial pressure, and increased the responsiveness of the sympathetic nervous system, as assessed by the slope of the regression line relating the increase in plasma norepinephrine concentration to the decrease in mean arterial pressure. These increases were accompanied by a decrease in the slope of the regression line relating the decrease in mean arterial pressure to the dose of sodium nitroprusside and thus were associated with a decreased sensitivity to the vasodepressor effects of sodium nitroprusside. These observations suggest that captopril's antihypertensive mechanism of action in hypertensive subjects with normal or low plasma renin activity does not involve an impairment of the sympathetic neuronal release of norepinephrine. (Hypertension 8: 229-237, 1986) KEY WORDS • renin-angiotensin system • sympathetic nervous system • plasma norepinephrine concentration • baroreflex sensitivity • angiotensin converting enzyme inhibition C APTOPRIL effectively decreases blood pressure by decreasing total peripheral resistance,' although the factors responsible for this vasodilation are unknown. A reasonable assumption, however, is that captopril-induced vasodilation could result from either the blockade of one or more endogenous vasoconstrictor systems or the amplification of one or more endogenous vasodilator systems.Because captopril is an orally active inhibitor ofFrom the

The effects of ramipril on sympathetic nervous system function in older patients with hypertension

“…Plasma norepinephrine levels were also found to be decreased in patients with hypertension treated with quinapril, 7 captopril, 21 or single‐dose benazepril 8 . Other studies have failed to identify changes in plasma norepinephrine level immediately following 22 , 23 , 24 or after short‐term 25 , 26 ACE inhibitor therapy.…”

Brain angiotensin II and baroreceptor reflex function in spontaneously hypertensive rats.

“…34 It has also been shown that captopril augmented baroreceptor reflex control of heart rate in response to a decrease in blood pressure in hypertensive patients. 35 In the latter study, baroreceptor reflex sensitivity to an increase in blood pressure was not examined. Mancia et al, 36 however, found that baroreceptor reflex activity was enhanced in response to a decrease in blood pressure but unaltered in response to an increase in blood pressure in hypertensive patients.…”

Converting‐enzyme inhibition buffers the counter‐regulatory response to acute administration of nicardipine.

“…However in this situation, it is difficult to dissociate the role of haemodynamic improvement from angiotensin II adrenergic facilitation. Recently the reflex sympathetic activation which accompanies infusion of sodium nitroprusside has been used to investigate whether angiotensin II controls noradrenaline in normotensive men (Becker et al, 1986) or in hypertensive patients (Clementi et al, 1986), by comparing its effects in the presence and in the absence of captopril. The interpretation of these results was that captopril does not impair the sympathetic nerve activity.…”