Lung Perfusion with Angiotensins I and II

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Abstract
Perfusion of isolated rat and guinea pig lungs with angiotensin I or II in Krebs' solution results in significant losses of peptide activity. This was not prevented by angiotensin cofactor. In addition to being converted to the octapeptide during passage through the lung, angiotensin I released a myotropic substance which is different from serotonin, epinephrine, norepinephrine, and prostaglandin E1 and F2α. This substance was not one of the several fragments of angiotensin I tested. There was a decreased responsiveness of rabbit aorta following repeated exposure to lung perfusate containing angiotensin I. Since repeated direct exposure to this peptide and metabolic fragments in Krebs' solution did not produce this effect, it was assumed to be caused by a substance released from the lungs.

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