SHOCK POTENTIATING ACTIONS OF ANGIOTENSIN-II INFUSION IN CATS

  • 1 January 1980
    • journal article
    • research article
    • Vol. 7  (3) , 343-351
Abstract
Anesthetized cats were infused with angiotensin II or its vehicle (0.05 M phosphate buffer) to detect actions of angiotensin II which can contribute to shock. Mild hemorrhage or saralasin-induced angiotensin II receptor blockade were employed to enhance or reduce the angiotensin II effects. Angiotensin II produced a prolonged reduction in superior mesenteric artery blood flow (50% of initial) and an elevation in plasma lysosomal hydrolase (cathepsin D) activity. Angiotensin II disrupted the normal functioning of the coronary endothelium, resulting in macroscopically visible hemorrhagic patches on the myocardium. Saralasin blockade of the angiotensin II receptor prevented the pressor, splanchnic vasoconstrictor and lysosomal labilizing actions of angiotensin and decreased the incidence of cardiac hemorrhages. Angiotensin II infusion after bleeding to 80 mm Hg increased lysosomal hydrolase release, indicating an exacerbation of angiotensin II effects. High levels of angiotensin II evidently are capable of inducing alterations similar to those occurring in hemorrhagic shock. These deleterious effects of angiotensin II were abolished by saralasin and potentiated by a mild hemorrhage.