Acute effect of an alpha 1-adrenoceptor antagonist on urinary sodium excretion, plasma atrial natriuretic peptide, arginine vasopressin, and the renin-aldosterone system in healthy subjects.

Abstract

To elucidate the mechanism underlying the sodium retention caused by alpha 1-adrenoceptor blockade in man, a placebo-controlled, randomised, double-blind study has been made of the acute effects of bunazosin an alpha 1-antagonist, on urinary sodium excretion, atrial natriuretic peptide (ANP), arginine vasopressin (AVP), and the renin-aldosterone system in 7 healthy men. A single oral dose of bunazosin 2.0 mg caused a significant reduction (P less than 0.05) in urinary sodium excretion after 0-2 h, 2-4 h, and 4-6 h. The mean values for plasma ANP, AVP, aldosterone, and cortisol concentrations at those times were similar after placebo and bunazosin, and plasma renin activity was significantly increased 2 and 4 h after bunazosin. Pretreatment with oral enalapril 10 mg, an angiotensin converting enzyme inhibitor, did not prevent the bunazosin-induced reduction in urinary sodium excretion. There was a significant positive correlation between the drug-induced changes in blood pressure and urinary sodium excretion. The results suggest that ANP, AVP, and renin-aldosterone may play little role in the sodium retention caused by acute alpha 1-adrenoceptor blockade in man.