Angiotensin, @entity519 , XXXX and pulmonary vessels.

@entity235 @entity1855 @entity1808 @entity519 @entity460 @entity3774 @entity35 @entity468
1. The action of @entity1808 on lung vessels was compared in @entity235 , @entity468 , ferrets and @entity35 using isolated perfused lungs and lobes of lungs perfused in vivo, both at constant flow, so that increases in inflow pressure at constant outflow pressure indicated increases in resistance. 2. @entity1808 caused some increases in resistance in @entity235 , @entity468 and @entity35 but not ferrets. The increases were small compared with changes in the systemic circulation. Larger increases could be obtained in isolated lungs where there was no interference from rises in left atrial pressure. 3. All four species showed pulmonary vasoconstriction during @entity519 and ferret lungs were especially responsive. Thus @entity1808 cannot be the mediator of @entity519 vasoconstriction in all these species. 4. @entity1808 significantly increased the response to @entity519 in isolated cat and @entity35 lungs while also increasing baseline inflow pressure; the response to @entity519 was not altered in ferrets. @entity1808 may therefore enhance reactivity of pulmonary vessels. 5. @entity1855 , an inhibitor of @entity460 transport across cell membranes, reduced the response to @entity519 in @entity35 and ferrets more than it reduced the response to @entity1808 in @entity35 or @entity3774 in ferrets. Thus @entity519 pulmonary vasoconstriction probably involves transport of @entity460 .
