Angiotensin I conversion and coronary constriction by angiotensin II in ischemic and hypoxic isolated rat hearts (original) (raw)

1991, European Journal of Pharmacology

Dose-response curves of angiotensin I (AI, l.O-1000.0 pmol) and angiotensin II (AR, 1.25-1250.00 pmol) were obtained in isolated rat hearts subjected to control conditions, mild hypoxia (PO, = 145 mm Hg), reoxygenation, ischemic (perfusion pressure = 3.5 mm HgI and reperfusion. Both AI and AI1 caused dose-dependent coronary vasoconstrictioc in control hearts, with a maximal reduction of coronary flow (CFI of 26 f 3 and 27 f 2%, respectively. The effects of both AI and AI1 were substantially attenuated during hypoxia, but were fully restored upon reoxygenation. During ischemia, the effect of AI1 was unaltered while the effect of AI was enhanced compared to the control (P < 0.05). This enhancement was reversible on reperfusion. Cardiac conversion of AI, calculated from ED,, values for AI and AII, was significantly increased during ischemia (P < 0.05). Infusion of saralasin (0.5-5.0 pg/minI did not increase CF in any of the groups. We conclude that (1) the coronary vasoconstrictive effect of AI1 is preserved in ischemia but attenuated in hypoxia and (21 cardiac conversion of AI to AI1 is enhanced in hearts injured by ischemia.