Cardiac contractility and sarcolemmal calcium binding in several cardiac muscle preparations

Abstract

Striking correlations are found between cardiac contractility and Ca2+ binding to isolated cardiac sarcolemma in rabbit, neonatal rat, and frog ventricular tissue. Deviations from this correlation are seen in the adult rat ventricle and rabbit atrium. The observation of this correlation in the three former tissues and under various ionic conditions suggests that this correlation is not coincidental and that Ca2+ bound to the cardiac sarcolemma is of major importance in the control of myocardial contractility. The data are consistent with a functional Ca2+-induced Ca2+ release system in the sarcoplasmic reticulum (SR) of all the tissues (which is controlled by Ca2+ entry from sarcolemmal sites), with the adult rat ventricular and rabbit atrial SR Ca2+ release being much more sensitive to CA2+. It is suggested that the frog, neonatal rat, and rabbit ventricles depend more directly on the entry of Ca2+ from sarcolemmal sites for the control of tension development, whereas the adult rat ventricle and rabbit atrium depend to a greater extent on CA2+ released from the SR.

Influence of polymyxin B, a probe for anionic phospholipids, on calcium binding and calcium and potassium fluxes of cultured cardiac cells.

“…The influence of PXB on Ca fluxes is of interest. The observed slowing of Ca uptake (^0.1 mM PXB) is consistent with observations correlating the quantity of Ca bound to the membrane with cell contractility and the magnitude of Ca influx (Bers and Langer, 1979;Bers et al, 1981). Control of Ca binding and flux resides in both the glycocalyx and the lipid bilayer, whereas control of K permeability resides only at the bilayer .…”

“…Furthermore, convincing evidence was provided that, rather than binding to the protein or saccharide moieties of the membrane, PXB (at 0.1 mM) interacts preferentially with the lipid moiety, specifically the anionic phospholipids. Since the anionic phospholipids are the major site of Ca binding in cardiac tissue (Philipson et al, 1980), and since Ca binding is directly related to the contractility of this tissue (Bers and Langer, 1979;Bers et al, 1981), PXB may be a useful probe for study of the role of this component in the control of transsarcolemmal Ca and K movements and Ca binding. The results of the present study support this possibility.…”

“…(Circ Res 53: 679-687, 1983) THE influence of membrane composition on membrane function has been the center of considerable interest in recent years Friend, 1980, 1982;Ponce-Hornos et al, 1982;Roelofsen and Van Deenen, 1973). In the field of cardiac cell function, this interest has centered on the role{s) of the glycocalyx and phosphospholipids in the binding of Ca and in the control of transmembranous ion fluxes (Bers et al, 1981;Frank et al, 1977;Langer and Nudd, 1980;Philipson et al, 1980). Exploration of the roles of the various classes of phospholipids has been limited by the absence of a probe which would specifically bind to, or alter, this membrane component.…”

Subcellular localization of the delayed rectifier K+channels KCNQ1 and ERG1 in the rat heart

“…Because the T tubule is the membrane structure predominating in excitation-contraction coupling (5,6,14,39,47,50,56,62), it is fascinating to speculate that the role of the sarcolemmal KCNQ1 channels is distinct from the T-tubular KCNQ1 channels. Whereas the most obvious function of T-tubular KCNQ1 channels is to counteract and overrule the depolarizing action of the Ca 2ϩ currents (DHPR) during the repolarization of the cardiac action potential, the sarcolemmal KCNQ1 channels could play another role.…”

Oxygen free radicals and calcium homeostasis in the heart

“…The sources of Ca 2+ that enters the cell across the sarcolemma are considered to be the extracellular space and Ca 2*-binding sites within the sarcolemmal membranes [24][25][26]. Langer et al [24][25][26] reported that membrane bound Ca 2+ in cardiac cell is a superficial store of Ca 2 § which becomes available for entry upon excitation of the myocardium.…”