Contractile responses of myocardium and vascular smooth muscle to angiotensin II were studied in isolated rabbit papillary muscles and aortic helical strips, with respect to the sensitivity and the mechanism of action. All experiments were performed in HCO3-buffered Tyrode solution which was aerated with 3% CO2-97% O2 and kept pH 7.35 at 35℃. Action potentials were measured by conventional microelectrode technique in the papillary muscles. Helical strips of vascular smooth muscle were prepared from the descending thoracic aorta of the rabbit. Angiotensin II elicited a positive inotropic effect in doses from 10-8 to 10-6 M, and this effect was dose-dependent and characterized by a symmetrical increase of maximum dP/dt during contraction and relaxation phase. Slow responses (or slow action potentials) were induced by A. II (10-6 M) in the papillary muscle hypopolarized by 27 mM K+. These A. II-induced slow action potentials were eliminated by verapamil (2 mg/l), but not affected by propranolol (10-5 M). In aortic helical strips, contractile force was increased dose-dependently in the range of 10-10 ~ 10-7 M A. II. ED50 in aorta was 3 X 10-9 M A. II, whereas that in paillary muscle was 2.5 X 10-7 M A. II. A. II contracted vascular smooth muscle in depolarizing concentration of K+ (100 mM K+), and also produced a sustained contraction even in the presence of verapamil and regitine. The results of this experiment suggest that the primarily important physiological role of A. II is the action on the blood vessel, and the positive inotropic effect of A. II in papillary muscle results from the increase of slow inward Ca++ current, and that A. II-induced contraction of aorta is independent of transmembrane potential and associated with promoting bet transmembrane Ca++-influx and the mobilization of cellular Ca++.
