SLOW INWARD CURRENT AND CONTRACTION IN FROG ATRIAL MUSCLE AT VARIOUS EXTRACELLULAR CONCENTRATIONS OF NA AND CA IONS

NaCa antagonism in frog cardiac muscle was investigated under voltage-clamp conditions to obtain further information about the underlying mechanism(s). Specifically the relationship between the slow inward current (Islow) and that part of contractility activated by this current (phasic tension) was examined in various [Na]0 and [Ca]0. When [Na]0 was reduced by substituting with LiCl or sucrose Islow was changed only slightly (decreased in LiCl and increased in sucrose), whereas, phasic tension was increased several fold regardless of the type of substitute. When [Ca]0 was reduced Islow was again less affected than phasic tension. This decrease in maximal peak tension resulting from reduced [Ca]0 was partially but not fully compensated for by simultaneously decreasing [Ca]0 and [Na]0, while keeping the ratio [Ca]0 [Na]02 constant. The current decreased almost immediately upon application of these low Na, low Ca solutions but the change in phasic tension was biphasic-an increase followed by a decrease. The results indicate that contractile force in frog myocardium does not simply depend on [Ca]0 [Na]02. The NaCa antagonism is explained by an interaction between the slow inward current and the intracellular stores of Ca which are regulated by NaCa exchange. A qualitative model of regulation of cardiac contractility is presented. © 1979.