Effects of ATP and vanadate on calcium efflux from barnacle muscle fibres

Abstract

Ca2+ carry the inward current during depolarization of barnacle muscle fibers and are involved in the contraction process. Intracellular ionized Ca ([Ca2+]i) in barnacle muscle, and in other cells, is kept at a very low concentration, against a large electrochemical gradient. This large gradient is maintained by Ca2+ extrusion mechanisms. When [Ca2+]i is below the contraction threshold, Ca2+ efflux from giant barnacle muscle fibers is largely ATP dependent and external Na+ (Na+o) dependent. When [Ca2+]i is raised to the level expected during muscle contraction (2-5 .mu.M), most of the Ca2+ efflux from perfused fibers is Nao dependent; as in squid axons, this Na+o-dependent Ca2+ efflux is ATP independent. Orthovanadate is an inhibitor of (Na+ + K+)ATPase and the red cell Ca2+-ATPase. Vanadate inhibited ATP-promoted, Na+o-dependent Ca2+ efflux from barnacle muscle fibers perfused with low [Ca2+]i (0.2-0.5 .mu.M), but has little effect on the Na+o-dependent, ATP-independent Ca2+ efflux from fibers with a high [Ca2+]i (2-5 .mu.M). ATP depletion or vanadate treatment of high [Ca2+]i fibers causes an approximately 50-fold increase of Ca2+ efflux into Ca2+-containing Li seawater. Vanadate and ATP affect Ca2+ extrusion, including the Na+o-dependent Ca2+ efflux (Na-Ca exchange), in barnacle muscle.