Effect of captopril on renin and blood pressure in cirrhosis

Summary In hepatic cirrhosis neurohumoral vasoconstrictor systems are activated to compensate for circulatory disturbances. To study the renin-angiotensin-aldosterone system in more detail, angiotensin converting enzyme in 15 patients with advanced liver disease was inhibited with captopril after moderate sodium restriction.Captopril caused an increase in plasma renin activity (p<0.005) and a decrease in plasma aldosterone (p<0.025) from an elevated baseline, and a moderate drop in systolic (p<0.025) and diastolic (p<0.05) blood pressure. Hyperreninaemia after captopril was inversely related to the prevailing plasma sodium level (r=–0.66,p<0.01), and the changes in both systolic and diastolic blood pressure were correlated with baseline plasma renin activity (r=0.49,p<0.05 for systolic andr=0.71,p<0.01 for diastolic blood pressure). No change occurred in heart rate or in stimulated plasma noradrenaline and vasopressin levels.The data suggest that in these cirrhotic patients the reactivity of the renin-angiotensin-aldosterone system was still intact, although it occurred at a higher level. They confirm the importance of the renin-angiotensin-aldosterone system in arterial blood pressure regulation in cirrhosis.