Response of the kidney to furosemide. II. Effect of captopril on sodium balance

Abstract

We investigated the role of the renin-angiotensin-aldosterone (RAA) system during furosemide (F) administration. The effects of adding captopril (C) (25 mg · 6 hr-1) to F (40 mg daily for 3 days) were studied in six normal subjects equilibrated to a daily sodium (Na) intake of 270 mmoles. Without C, F produced a marked natriuresis but Na+ excretion fell sharply between drug doses. This resulted in neutral Na balance (+22 ± 58 mmoles · 3 days-1; mean ± SE). Plasma angiotensin (AII) and aldosterone (Aldo) rose, but mean blood pressure (MBP) was unaltered. C abolished the F-induced increases in AII and Aldo but did not modify the pattern of Na+ excretion. Na+ balance remained neutral (+42 ± 54 mmoles · 3 days-1). With C alone, Na+ balance was positive (+110 ± 30 mmoles · 3 days-1; P < 0.02). In protocols C alone and F + C, MBP fell by a comparable amount. F alone and F + C increased plasma norepinephrine and prostaglandin E2 metabolite; these did not change with C alone. In conclusion, activation of the RAA system by F is not essential for the compensatory increase in Na+ reabsorption that maintains Na+ balance after F. Sympathetic nervous system activation or changes in prostaglandin E2 release may contribute to the increased Na+ reabsorption that follows the acute natriuresis induced by F.