Research Information System
Prostaglandines and Medicine, vol.2, no.5, pp.343-352, 1979 (SCI-Expanded)
The change of activity of angiotensins I and II was studied in the isolated perfused rat lung. Rabbit aorta and rat stomach fundus were used as test organs and continuously superfused with the venous effluent of the lung. In the presence of acetyl salicylic acid angiotensin I given through the pulmonary artery induced an augmentation in perfusion pressure and rabbit aorta contractility when compared with that of controls. There was no change observed for angiotensin II in both parameters. The responses to both peptides in the rat stomach fundus were significantly decreased after acetyl salicylic acid. Further addition of PGE2 to the perfusion medium caused a recovery of these responses. PGE2 alone did not alter the control responses to the peptides. Converting enzyme inhibitor, SQ 20.881, caused a significant inhibition in the responses to angiotensin I measured in perfusion pressure and rabbit aorta without altering that of angiotensin II in both parameters. However, this nonapeptide significantly potentiated the responses to both peptides in the rat stomach fundus. These data were taken as evidence for a possible relation between the converting enzyme and PG-synthetase, thus the inhibition one of these enzymes by its specific inhibitor causes activation of the other enzyme. These data also indicate that endogenous prostaglandins may inhibit the conversion of angiotensin I to angiotensin II in the pulmonary circulation. © 1979.