Gentilini P, Romanelli R G, La Villa G, Maggiore Q, Pesciullesi E, Cappelli G, Casini Raggi V, Foschi M, Marra F, Pinzani M
Clinica Medica II, University of Florence School of Medicine, Italy.
Gastroenterology. 1993 Feb;104(2):588-94. doi: 10.1016/0016-5085(93)90431-b.
In cirrhotic patients with ascites, captopril has deleterious effects on renal function, which have been referred to as captopril-induced arterial hypotension. The effects of this drug on renal function in cirrhosis were evaluated using low-dose captopril, thereby avoiding any change in arterial pressure.
In a randomized, double-blind, placebo controlled, cross-over trial, the effects of 12.5 mg captopril on renal plasma flow, glomerular filtration rate (measured by radioisotopic techniques), and sodium excretion in healthy controls and cirrhotic patients with and without ascites were determined.
In healthy subjects, captopril only induced a significant, 18% increase in renal plasma flow. In contrast, glomerular filtration rate significantly decreased in patients with (from 108 +/- 7 to 78 +/- 9 mL/min) and without ascites (from 102 +/- 4 to 88 +/- 3 mL/min), whereas renal plasma flow did not change. Urinary sodium excretion also significantly decreased in ascitic patients (from 43.8 +/- 4.4 to 30.6 +/- 3.8 mumol/min).
These data suggest that angiotensin II contributes to maintain renal hemodynamics in cirrhosis with and without ascites.
