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 also employed in an attempt 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. Additionally, 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 also decreased the incidence of cardiac hemorrhages. Angiotensin II infusion after bleeding to 80 mmHg, however, increased lysosomal hydrolase release, indicating an exacerbation of angiotensin II effects. These data indicate that high levels of angiotensin II 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.
|Original language||English (US)|
|Number of pages||9|
|State||Published - Jan 1 1980|