ANGIOTENSIN-II MODULATES THE DELAYED RECTIFIER POTASSIUM CURRENT OF GUINEA-PIG VENTRICULAR MYOCYTES

Amplitude of the delayed rectifier (I-K) tail current measured following long (5000msec) depolarizing pulses (-10 to +50mV) was decreased 19 +/- 3 % (P < 0,05) in a voltage-independent manner by angiotensin II (AII) 100nM. In contrast, amplitude of tail current measured following short (250msec) depolarizing pulses to potentials > +10mV was increased 13+/-3 % (F < 0.05) by AII 30nM. Deactivation kinetics of I-K measured at -30mV were altered by AII 30nM and 100nM; time constant of the faster deactivating phase (tau(1)) was decreased 1.4-fold. In summary, data obtained demonstrated that physiological concentrations of AII modulates major outward potassium currents involved in cardiac repolarization. Results suggest that AII increases amplitude of the rapid component of I-K (I-Kr) but decreases its slow component I-Ks. Thus, we postulate that modulators of AII effects may exhibit direct cardiac electrophysiological properties.