To examine the possible contribution of the renin-angiotensin-aldosterone system to portal hypertension in patients with cirrhosis of the liver, seven such patients were studied with the hepatic venous catheterization technique, in the basal state, and after the intake of 12.5 to 25 mg of captopril. Hepatic venous wedge pressure was 22 +/- 2 mm Hg in the basal state and fell to 19 to 20 mm Hg at 45 to 90 minutes after the administration of captopril (P less than 0.05 to 0.01). Wedge to free hepatic venous pressure difference (basal 14 +/- 2 mm Hg) remained unchanged after captopril, and estimated hepatic blood flow was unaltered. Small but significant reductions in arterial blood pressures were seen after the administration of captopril. Aldosterone concentrations decreased whereas renin activity tended to increase after captopril. It is concluded that captopril inhibits the renin-angiotensin system in patients with cirrhosis of the liver, but fails significantly to decrease portal venous pressure. Captopril is thus unlikely to favorably influence the incidence of bleeding in these patients.