CHANGES IN GLOMERULAR-FILTRATION RATE AND RENAL PLASMA-FLOW IN CIRRHOTIC RATS DURING CONVERTING-ENZYME INHIBITION

During the development of cirrhosis ascites-edema, peripheral vasodila tation, hypotension and an increase of the plasma concentration of sev eral neurohormones are frequently observed. Such complex changes in th e hormonal profile hinders the assessment of the relative role of each in the pathophysiology of this disease. The purpose of this work was to evaluate in a rat model of experimental cirrhosis (phenobarbital/CC l4 the role of the renin-angiotensin system in the preascitic stage of the disease using the converting enzyme inhibitor captopril. Cirrhoti c rats showed diminished renal and hepatic perfusion. Compared to norm al rats, glomerular filtration rate in cirrhotic rats was reduced fr o m 0.75 +/- 0.11 to 0.42 +/- 0.06 mL/min/100 g BW, and renal plasma flo w was reduced from 2.37 +/- 0.28 to 1.58 +/- 0.16 mL/min/100 g BW, the indocyanine green slope changed from - 0.095 +/- 0.028 to -0.057 +/- 0.01; the plasma sodium concentration fell from 144 +/- 1.5 to 131 +/- 5.40 mEq/L (all <.05). The mean arterial pressure was not reduced in the cirrhotic rats. There was no ascites. Both the acute (25 mg i.v.) and chronic (25 mg i.p. daily plus 25 mg/L in drinking water) administ ration of captopril to cirrhotic rats induced an increase in glomerula r filtration rate and renal plasma flow along with a steeper slope in indocyanine green decay (p <.05 for all three parameters) when compare d to non-treated cirrhotic animals. No changes were observed in contro ls. In the balance studies, an increase in urinary volume along with a decrease in urinary osmolality was recorded in cirrhotic rats on chro nic captopril treatment. In conclusion, our results show an activation of the renin-angiotensin system in these rats, as disclosed by the in hibition of the converting enzyme, as well as a possible interaction w ith ADH.