Effects of angiotensin I and antiotensin II on canine hepatic vascular resistance.

The effects of angiotensin I (0.2-3.2 ju.g) and angioteasin II (0.1-1.6 fig) injections into the pump-perfused arterial supply of the liver were studied in dogs anesthetized with sodium pentobarbital. Marked increases in hepatic artery perfusion pressure (10—50%), reflecting directicnally similar changes in resistance to blood flow, were caused by either angiotensin I or angiotensin II. Resistance increases produced by angiotensin I were significantly attenuated by the synthetic nonapeptide SQ 20881 (Pyr-Trp-Pro-Arg-Pro-Gln-Iie-Pro-Pro, 50 j«,g/kg, iv) that inhibits enzymatic conversion of angiotensin I to ang:otensin II. In contrast; responses caused by angiotensin II were unaltered by SQ 20881. However, resistance increases caused by either angiotensin I or angiotensin II were blocked by 1-Sar8-Ala-angiotensin II (100 /ug/kg mirr, ia), a specific angiotensin II antagonist. These findings parallel the finding that responses to angiotensin I in the vasculature supplied by the hepatic artery are largely caused by local enzymatic conversion of angiotensin I to angiotensin II. Such conversion appears to occur to the extent of about 46$.