Effect of dietary sodium intake on the pressor reactivity to angiotensin II in rats with experimental cirrhosis of the liver

Abstract

The present experiments were designed to evaluate vascular reactivity to angiotensin II in rats with experimental cirrhosis of the liver (induced with CCl4 and phenobarbital) before ascites appearance. The systemic pressor response to angiotensin II in conscious animals and the contractile effect of angiotensin II in isolated femoral arteries were studied. In addition, the effect of high sodium intake on these parameters was also analyzed. Both renin and aldosterone plasma concentrations were similar in control and cirrhotic rats on the normal or on the high sodium diet. Basal mean arterial pressure was higher in control rats than in cirrhotic rats on the normal sodium (116 ± 4 vs. 101 ± 4 mmHg (1 mmHg = 133.3 Pa),p < 0.05) or on the high sodium diet (118 ± 7 vs. 98 ± 6 mmHg). No differences in plasma renin activity or plasma aldosterone were found between control and cirrhotic rats. Upon injection of angiotensin II, control rats show a dose-dependent increase in mean arterial pressure which is higher in high sodium than in normal sodium rats. Cirrhotic rats showed a lower hypertensive response to angiotensin II than their corresponding control rats. In addition, no difference between pressor responses to angiotensin II was observed when normal sodium and high sodium cirrhotic rats were compared. On application of angiotensin II, femoral arteries of control and cirrhotic rats exhibited a dose-dependent contraction. However, maximal contraction was higher in high sodium control rats (145 ± 12 mg) than in normal sodium control rats (99 ± 6 mg, p < 0.05). No significant differences between control and cirrhotic rats on either sodium diet were observed. In conclusion, cirrhotic, nonascitic rats showed an impaired pressor response to angiotensin II that is more marked after a high sodium diet. These differences are not due to changes in the contractility of peripheral arteries to angiotensin II.Key words: angiotensin II, liver cirrhosis, sodium intake, mean arterial pressure, vascular reactivity.