Effects of angiotensin on pulmonary and systemic hemodynamics

Publisher Website
Google Scholar
Abstract
In ten morphine-urethan anesthetized dogs single injections of 2.0 µg/kg of synthetic valine 5 angiotensin II amide elevated systemic and pulmonary arterial pressures and depressed heart rate. Thirty-minute intravenous infusions of angiotensin (0.4 and 1.0 µg/kg/min) in eight dogs elevated systemic arterial pressure and diminished heart rate. Pulmonary arterial, pulmonary wedge, left ventricular end-diastolic, and right atrial pressures were all slightly elevated; mean cardiac output did not change. Calculated total pulmonary resistance and pulmonary arterial resistance were diminished; central blood volume was elevated. These findings suggest that elevated systemic pressure and resistance increase myocardial work and induce reflex bradycardia, thereby elevating left ventricular end-diastolic, pulmonary wedge, and pulmonary arterial pressures. Systemic vasoconstriction also contributes to the elevated right atrial pressure and distention of the pulmonary vascular bed, which diminishes total pulmonary and pulmonary arterial resistance. These findings are not incompatible with the theory that the renin-angiotensin system is active in essential hypertension.