Electromechanical effects of angiotensin in human atrial tissues.

Effects of exogenous angiotensin I (AI) and angiotensin II (AII) on action potential and contractile force of isolated atrial trabeculae obtained at cardiac surgery were studied by means of a standard microelectrode technique. In trabeculae driven electrically at a cycle length of 1 s, AII (8.4 nM - 8.4 microM) increased the contractile force with a peak effect occurred near 0.84 microM. The inotropic effect of AII was markedly inhibited by 1 microM saralasin or 1 microM diltiazem. AI (0.65 nM - 6.5 microM) also induced positive inotropic effect in a concentration-dependent manner. This inotropic effect was decreased significantly after 3 microM captopril pretreatment. In trabeculae active spontaneously in normal Tyrode solution, AI and AII increased significantly rate of diastolic depolarization and spontaneous discharges as well as force of contraction. These chronotropic effects were inhibited by captopril and saralasin, respectively. Captopril (0.3 nM - 3 microM) or saralasin (0.001 - 1 microM) alone also induced dose-dependent negative chronotropic effects. The present findings suggest the existence of functional AII receptors in human atrial tissues. The stimulatory effects of angiotensin appear to be related to an increase in cellular calcium.