title: Calcium, cell membrane, and excitation-contraction coupling.
abstract: Skeletal muscle, heart muscle, and smooth muscle differ with respect to morphology, function, and Ca metabolism. For the actual coupling between excitation and contraction, three different sources of Ca2+ supply are conceivable: release from intracellular organelles, release from plasmalemmal binding sites, and transmembranous influx. Considerable experimental evidence favors the membranes of the sarcoplasmic reticulum as the source of coupling Ca2+ in skeletal muscle, whereas in cardiac and smooth muscles the Ca store from which coupling Ca2+ is released has to be in intimate contact with the extracellular Ca2+ concentration. In order to distinguish between the two remaining possibilities for the source of coupling Ca2+, i.e., transmembranous Ca influx and Ca release from the plasmalemma, Ca antagonist--widely accepted tools for detecting Ca influx--were used. Ca antagonists did not have any influence on Ca exchange or Ca uptake either in cardiac or in smooth muscles. These findings may be interpreted as follows: Ca antagonists do not act by inhibiting the Ca2+ influx, although they reduce the amount of coupling Ca2+. This conclusion conflicts with current ideas concerning the mode of action of Ca antagonists. We feel, however, that the experimental support for the Ca-channel hypothesis is rather vague. This leads us to favor the plasmalemma as the main source of coupling Ca2+ in cardiac and smooth muscles.
mesh_terms: D000818:Animals; D001665:Binding Sites; D002118:Calcium / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism; D007473:Ion Channels / Q000378:metabolism; D008564:Membrane Potentials; D009119:Muscle Contraction; D009130:Muscle, Smooth / Q000378:metabolism; D009132:Muscles / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism
chemical_list: D007473:Ion Channels; D002118:Calcium