Angiotensin, hypoxia, verapamil and pulmonary vessels.

Abstract

1. The action of angiotensin II on lung vessels was compared in dogs, cats, ferrets and rats 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. Angiotensin II caused some increases in resistance in dogs, cats and rats 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 hypoxia and ferret lungs were especially responsive. Thus angiotensin II cannot be the mediator of hypoxic vasoconstriction in all these species. 4. Angiotensin II significantly increased the response to hypoxia in isolated cat and rat lungs while also increasing baseline inflow pressure; the response to hypoxia was not altered in ferrets. Angiotensin II may therefore enhance reactivity of pulmonary vessels. 5. Verapamil, an inhibitor of calcium transport across cell membranes, reduced the response to hypoxia in rats and ferrets more than it reduced the response to angiotensin II in rats or prostaglandin F2 alpha in ferrets. Thus hypoxic pulmonary vasoconstriction probably involves transport of calcium.