Length-dependent deactivation of ventricular trabeculae in the bivalve, Spisula solidissima |
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Authors: | L P Collis Y Sun R B Hill |
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Institution: | (1) Biocurrents Research Center, Marine Biological Laboratory, 7 MBL Street, Woods Hole, MA 02543, USA;(2) University of Rhode Island, Kingston, RI 02881, USA |
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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 μM) and blocked with high extracellular
Ca2+ (56 mM). The Ca2+ ionophore, A23187 (10 μM), augmented deactivation as did the positive inotrope serotonin (100 nM). Treatment with ryanodine
(5 μM) had no significant effect on deactivation. These results suggest that a reduction in Ca2+ at the contractile element and/or sequestration of Ca2+ 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 Ca2+ fluxes during sudden length perturbations may explain the effect of stretch on action potential duration in the bivalve heart,
as shown previously. |
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Keywords: | Bivalve Quick-release Shortening-deactivation Autoregulation Starling |
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