Effect of angiotensin‐ll blockade on systemic and hepatic haemodynamics and on the renin‐angiotensin‐aldosterone system in cirrhosis with ascites

Abstract

The effect of angiotensin-II blockade with saralasin on the cardiovascular and hepatic hemodynamics and on the renin-angiotensin-aldosterone system in 14 patients with cirrhosis and ascites, was studied. Control measurements showed that most of the patients had a low mean arterial pressure, high plasma volume, normal or high cardiac index, low peripheral resistance and high plasma renin activity and aldosterone concentration. The wedged hepatic venous pressure was increased in each patient and the estimated hepatic blood flow was normal in most of them. Overall, saralasin induced a significant reduction of the mean arterial pressure, cardiac index and peripheral resistance. The decrease of the peripheral resistance was greater than that of the cardiac index. Six of the patients developed a marked reduction of the mean arterial pressure with low doses of saralasin 1-2.5 .mu.g/kg per min and they had significantly higher plasma renin activity and lower mean arterial pressure than the remaining 8 patients who showed a slight or no hypotensive response in spite of infusing saralasin up to a dose of 10 .mu.g/kg per min. The decrease of the mean arterial pressure correlated directly with the baseline values of plasma renin activity. Angiotensin-II blockade induced a significant reduction of the wedged hepatic venous pressure. The hepatic blood flow did not show any significant change. The decrease of the wedged hepatic venous pressure was directly related to the reduction of the mean arterial pressure and also to the control plasma renin activity. In most patients with cirrhosis, ascites and high plasma renin activity, arterial pressure is apparently maintained by the effect of endogenous angiotensin II on the peripheral vasculature. A pre-existing arterial hypotension secondary to an arteriolar vasodilatation is probably the cause of renin release in these patients. Angiotensin-II blockade is apparently accompanied by a reduction of the postsinusoidal hepatic vascular resistance.