Abstract
The actions of Sr2+ on the smooth muscle of the guinea pig taenia coli were studied under constant-current and voltage-clamp conditions. In replacing Ca2+, Sr2+ (2.5 mM) prolongs the duration of the action potential by slowing the rate of repolarization, but increases the steady-state membrane conductance. These changes occur in preparations in Krebs solution as well as in preparations in a Na+-free tetraethylammonium medium. When [Sr2+]o [external Sr2+ concentration] is increased to 20 mM, the amplitude of the spike is increased, and the duration shortened. Under voltage-clamp conditions, Sr2+ carries the early inward current (Ia). Increasing [Sr2+]o increases the maximum Ia and shifts its reversal potential (Ea) towards more positive voltages without affecting the conductance, .hivin.ga. Sr2+ does not affect the steady-state inactivation of Ia, but markedly slows the rate of inactivation. In all concentrations, Sr2+ enhances the late outward current (Ib, chiefly Ik), by increasing the conductance, .hivin.gb. The degree of increase is greater in higher [Sr2+]o. Ca2+ at concentrations of 1 or 2.5 mM added to Sr2+ solutions partially reverses the above effects, suggesting the presence of some competition for the same channel or binding sites or both. In the taenia coli, there is a component of the K+-conductance system which is sensitive to [Sr2+]o and to [Ca2+]o [external Ca2+ concentration]. The inactivation of the early inward current is an important mechanism underlying the repolarization of the action potential and IK probably has a delayed and gradual onset.