Abstract
1. The effect of adrenaline on the Ca-dependent slow inward current, Is, of mammalian cardiac muscle has been investigated by the voltage-clamp method. The mechanism of the increase in the conductance, gs, was analysed on the basis of a kinetic scheme (Hodgkin & Huxley, 1952) applicable to this system. 2. The rate constants alphad and betad, of activation of gs were not influenced by adrenaline, although the limiting conductance, gs, was greatly increased. 3. Reduction of [Ca]o 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. This indicates that the catecholamine has no influence on the selectivity of these conductance channels. 4. An increase in the number of functional conductance channels by adrenaline is discussed as a possible mechanism for the increase in Gs.
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