The regulation of the calcium conductance of cardiac muscle by adrenaline.

Abstract

The effect of adrenaline [epinephrine] on the Ca-dependent slow inward current, Is, of mammalian cardiac muscle [ventricular trabeculae from cow hearts and papillary muscles from cat hearts] was investigated by the voltage-clamp method. The mechanism of the increase in the conductance, gs, was analysed on the basis of a kinetic scheme applicable to this system. The rate constants, .alpha.d and .beta.d, of activation of gs were not influenced by adrenaline, although the limiting conductance, .hivin.gs, was greatly increased. Reduction of [Ca]o [external Ca concentration] from 1.8 to 0.2 mM decreased the amplitude of inward tail currents when gs was fully activated; however, the relative decrease of the current amplitude was the same with and without adrenaline. The reversal potential, ER, of Is was not changed by the drug. The catecholamine appears to have no influence on the selectivity of these conductance channels. An increase in the number of functional conductance channels by adrenaline is discussed as a possible mechanism for the increase in .hivin.gs.