Angiotensin II modulates the delayed rectifier potassium current of guinea pig ventricular myocytes.

Amplitude of the delayed rectifier (IK) 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% (P < 0.05) by AII 30nM. Deactivation kinetics of IK 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 IK (IKr) but decreases its slow component IKs. Thus, we postulate that modulators of AII effects may exhibit direct cardiac electrophysiological properties.