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Updated: Aug 7, 2026

Analysis of Tubular Membrane Networks in Cardiac Myocytes from Atria and Ventricles
Published on: October 15, 2014
Control of ion movement by cardiac sarcolemma
Abstract:
The cation affinity sequence based on 45Ca displacement from neonatal rat heart tissue culture cells was La greater than Cd greater than Zn greater than Mn greater than Mg. This sequence correlated with the rate at which these ions diminished contractile tension in neonatal rat papillary muscles. In adult rat interventricular septa elevated extracellular Mg diminished tension development concomitant with a decrease in 45Ca influx. The results support the hypothesis that these cations interfere with contraction by occupying sarcolemmal sites ordinarily reserved for calcium or by interfering with transmembrane Ca movements, both of which are crucial for tension development. The data of Bockman et al. (2) provides further support for this hypothesis. Elevated extracellular Mg reduced potassium exchange by 30% in adult rat interventricular septa but had no effect on 42K EXCHANGE IN CONTROL RABBIT INterventricular septa. Elevated extracellular Mg did inhibit the net 42K loss induced by digitalis glycoside without affecting tension development or glycoside inhibition of 42K influx in the rabbit heart. High Mg also attenuated the increase in 42K exchange produced by elevated extracellular potassium. These data demonstrate that glycoside inotropy is not dependent on potassium loss from myocardium but are consistent with the hypothesis that increased intracellular sodium mediates glycoside inotropy. A model for the effects of Mg in rat and rabbit heart is presented.
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