Reduced splanchnic vasoconstriction to angiotensin II in conscious rats with biliary cirrhosis.

Decreased pressor reactivity to angiotensin II has been demonstrated in portal hypertension due to cirrhosis. The present study investigated the respective roles of portal hypertension and cirrhosis and the hemodynamic mechanisms of the depressor response in different models of portal hypertension in conscious rats. Dose-pressor curves were studied in sham-operated, portal vein stenosed (portal hypertension without cirrhosis) and biliary cirrhotic rats following angiotensin II administration. Decreased pressor response was observed in cirrhotic rats but not in portal vein stenosed rats. The hemodynamic effects of angiotensin II administration (11 ng.100 g-1 body wt.min-1, i.v.) were studied in conscious sham-operated and biliary cirrhotic rats (radioactive microsphere method). The percentage of change from basal values following angiotensin II administration were significantly more marked in sham-operated rats than in cirrhotic rats for mean arterial pressure (+34 vs. +6%), cardiac index (-36 vs. -22%), systemic vascular resistance (+117 vs. +40%). After angiotensin II, portal tributary and hepatic artery blood flows significantly decreased in sham-operated rats (-31 and -14%, respectively) but not in cirrhotic rats (+1 and +23%), whereas changes in renal blood flow were not significantly different between the two groups (-44 vs. -34%). In conclusion, in biliary cirrhotic rats, decreased pressor response to angiotensin II depends on the presence of liver disease rather than on portal hypertension or basal hemodynamic alterations. It also depends on the decreased vasoconstrictive effect which predominates in the splanchnic vascular bed.