Inotropic and vasoactive effects of the naturally occurring angiotensins in isolated cat cardiac muscle and coronary arteries

Angiotensin (Angio) I, II and III were added to isolated cat papillary muscles and to isolated perfused coronary arteries. Angio II was the most potent of these, increasing contractile force 99 ± 7% at 10^-6 M. In contrast Angio III increased force development by 45 ± 5% and Angio I increased force 26 ± 4% at 10^-6 M. The positive inotropic response to Angio I was not significantly altered by converting enzyme inhibition (26 ± 4 vs. 28 ± 3%), indicating that Angio I can direcly influence ventricular contractility, without conversion to Angio II. Angio II and III produced comparable elevations of perfusion pressure in coronary arteries perfused at constant flow. Angio III (10^-6 M) increased perfusion pressure 39 ± 7 mm Hg compared to a 41 ± 7 mm Hg increase for Angio II at the same concentration. Angio I was a less potent constrictor of the coronary vasculature, increasing pressure 12 ± 2 mm Hg at 10^-6 M. This constrictor response was significantly reduced after converting enzyme inhibition to 5 ± 1 mm Hg, p<0.02. Angio II was the most potent of the three peptides, exerting strong positive inotropic and coronary vasoconstrictor effects above 10^-8 M. Angio I was the least potent of the three with regard to inotropic and coronary vasoconstrictor actions, the latter being dependent on conversion to Angio II. Angio III was less potent inotropically than Angio II but was similar to Angio II in its coronary vasoconstrictor activity. These effects of Angio I, II and III can be potentially dangerous in hemorrhagic shock or in acute myocardial ischemia.