Vascular and Aldosterone Responses to Angiotensin II in Normal Humans: Effects of Nicardipine

Abstract

The effects of the dihydropyridine calcium antagonist nicardipine on pressor responsiveness and hormone release were investigated in healthy normotensive men following both acute intravenous administration and 1 week of oral treatment. There were no significant changes in baseline supine blood pressures but the pressor responsiveness to the intravenous infusion of angiotensin II was significantly attenuated by both intravenous and oral nicardipine. This reduction tended to be greater following intravenous nicardipine, which achieved the highest mean plasma nicardipine concentrations. Neither intravenous nor oral nicardipine caused any significant differences in the aldosterone response to the angiotensin II infusion and there were no significant differences attributable to nicardipine in the levels of plasma renin activity. However, the progressive increase in the aldosterone/renin ratio observed during placebo was significantly attenuated by both nicardipine treatments. There were no significant effects on plasma cortisol, adrenocorticotropic hormone, or noradrenaline. This study has shown that nicardipine acutely and chronically reduces vascular responsiveness to the pressor effect of angiotensin II. There was no significant effect on the aldosterone response to angiotensin and no evidence of clinically significant interference with the release of other hormones to suggest that this mechanism contributes to the antihypertensive effect of nicardipine.