Cellular and subcellular mechanism of transient depolarization.

Abstract

Cardiotonic steroids cause single ventricular cells to exhibit transient depolarization after a train of driven action potentials or, in voltage clamp experiments, transient inward current after a depolarizing clamp pulse. Transient depolarization or transient inward current was eliminated by an intracellular injection of EGTA. Transient depolarization was elicited by an intracellular injection of CaCl2, even in the control Tyrode's solution. Together with transient depolarization or transient inward current, digitalis intoxication promoted spontaneous oscillatory fluctuations in membrane potential or in membrane current. Their power spectra peaked at frequencies of 3-4 Hz and coincided well with the frequency of repetitive transient depolarization. The fluctuations were eliminated by intracellular injections of EGTA and decreased in amplitude by caffeine with a shift toward higher frequencies. These result suggest that an oscillatory release of Ca from intracellular storage sites is the common basis underlying both the transient events and the spontaneous fluctuations in membrane potential or current. The Ca-sensitive current, measured by intracellular Ca injection, flowed inwardly at negative potentials and reversed polarity at around -22 mV. Therefore this current component is carried by more than one ion.