Low extracellular sodium concentration elevates cellular calcium content in isolated guinea-pig heart muscle, likely involving cellular stores that regulate twitch amplitude.
Should not change clinical practice; hypothesis-generating for Na+-dependent Ca2+ handling in cardiac muscle.
The effects of low extracellular sodium concentration [( Na+]0, 76 mmol/l) on force of contraction, transmembrane action potentials and on calcium, sodium and potassium contents were studied in guinea-pig heart muscle using sucrose or lithium as substitutes for sodium. In papillary muscle, the positive inotropic response to low [Na+]0 was accompanied by shortening in action potential duration, in atrial muscle, prolongation at 90% of repolarization was observed. After 30 min. in low [Na+]0 solution (Ca2+ 1.8 mmol/l), the net uptake of calcium in left atria was larger in sucrose- than in lithium-substituted solution, i.e. 0.45 and 0.2 mmol Ca2+/kg wet weight, respectively. The net sodium content decreased monophasically; but the potassium content did not change consistently. The uptake of lithium by the atria was at least partially compensated for by a loss in potassium and by a transient decrease in sodium content. Increase in stimulation frequency from 0.1 to 1 Hz accelerated the time course of change by a factor of 2. In low [Na+]0, post-rest adaptation of twitch tension appeared abolished in atria because of high amplitude contractions. The recovery pattern of post-rest twitch amplitude was greatly accelerated in papillary muscle. In conclusion, low [Na+]0 elevates the cellular calcium content; this extra calcium is probably located in cellular stores that are involved in the regulation of twitch amplitude.
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Lüllmann et al. (1991) studied this question.
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