Possible prostacyclin-mediated vascular effect of angiotensin II in the isolated perfused rat lung.

Angiotensin I (A I) and angiotensin II (A II) when injected through the pulmonary artery caused an increase in perfusion pressure (PP) of the isolated perfused rat lung and a contraction when the venous outflow was superfused over rat ascending colon (RC). Nicotine (N) when added to the perfusion medium caused a significant increase in PP to A II without altering that to A I. Further addition of ZK 36374, a stable analog of prostacyclin (PGI2), to the medium prevented the potentiating effect of N on the A II pressor response. Neither N nor ZK 36374 altered the superfused RC responses to A I and A II-injected venous effluent. Lysine acetylsalicylate (ASA), however, caused a potentiation in the pressor response to A I. The response of venous effluent superfused RC to A I was also found to be potentiated by ASA. ASA failed to alter the responses to A II. These results were taken as evidence that A II is a potent activator for the biosynthesis of PGI2 in the pulmonary vascular bed. Moreover, PGI2 does not affect angiotensin converting enzyme activity in the lung circulation while other stable metabolites of arachidonic acid can inhibit the conversion of A I to A II.