Effects of Angiotensin I and Angiotensin II on Canine Hepatic Vascular Resistance
The effects of angiotensin I (0.2-3.2 µg) and angiotensin II (0.1-1.6 µg) 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 directionally 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-Ile-Pro-Pro, 50 µg/kg, iv) that inhibits enzymatic conversion of angiotensin I to angiotensin 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-Sar-8-Ala-angiotensin II (100 µg/kg min-1, 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%.
- angiotensin antagonist
- angiotensin-converting enzyme
- hepatic arterial perfusion
- hepatic vasoconstriction
- local blood flow
- perfusion pressure
- Received April 24, 1972.
- Accepted October 30, 1972.
- © 1973 American Heart Association, Inc.