ABSTRACT
Shortening-deactivation has been identified and characterized in ventricular trabeculae of the bivalve, Spisula solidissima (Heterodonta, Mactridae). This muscle had ultrastructural similarities to vertebrate smooth muscle. Deactivation was defined as the fraction of maximal force lost during a contraction when a muscle is shortened rapidly (by a quick-release, QR) to a known length, relative to a control isometric contraction at that same length. The magnitude of deactivation was dependent on the size of the release and the point at which the release was applied during the cycle of contraction. QR/quick-stretch (QS) perturbations at the same point during the contraction resulted in negligible deactivation. The magnitude of deactivation was independent of shortening rate. Deactivation was attenuated by applying caffeine (100 microM) and blocked with high extracellular Ca(2+) (56 mM). The Ca(2+) ionophore, A23187 (10 microM), augmented deactivation as did the positive inotrope serotonin (100 nM). Treatment with ryanodine (5 microM) had no significant effect on deactivation. These results suggest that a reduction in Ca(2+) at the contractile element and/or sequestration of Ca(2+) may occur during shortening. Deactivation may minimize the magnitude of work done during active shortening of bivalve cardiac muscle, particularly against the low afterload exhibited in the bivalve peripheral circulatory system. Intracellular Ca(2+) fluxes during sudden length perturbations may explain the effect of stretch on action potential duration in the bivalve heart, as shown previously.