Abstract
Frog heart relaxation was analyzed under voltage clamp conditions as the tension decay observed after the membrane potential had been returned to its resting value. The tension decayed exponentially with a time constant of 188±3.8 ms SEM. The relaxation rate decreased with the external Na concentration. It fell to about one tenth in a Na-free solution. Increasing the intracellular Na-content by an application of veratrine also decreased the relaxation rate. Thus relaxation seems dependent on the Na gradient. The relaxation rate decreased within one second upon switching from a high to a low Na-containing solution. The relaxation rate reached a minimum before rising slightly to a new steady state value. This rebound may reflect the partial recovery of the Na gradient since a fast variation in [Na]i follows alteration of [Na]o. Mn and La ions also slowed relaxation. In a Na-free solution, adrenaline accelerated tension decay, an effect not noticeable in frog heart contained in Ringer solution. Other cAMP-promoting agents, such as dibutyryl-cAMP and aminophylline, also increased relaxation rate.
It is concluded that in frog myocardium, part of the decrease of the intracellular Ca2+-concentration which occurs during each cardiac cycle could be dependent on a Na−Ca exchange mechanism. The relative importance of this mechanism, versus internal Ca sequestration, in the relaxation of tension may well be greater in contractile tissues whose cells have a large surface/volume ratio.
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Roulet, MJ., Mongo, K.G., Vassort, G. et al. The dependence of twitch relaxation on sodium ions and on internal Ca2+ stores in voltage clamped frog atrial fibres. Pflugers Arch. 379, 259–268 (1979). https://doi.org/10.1007/BF00581430
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DOI: https://doi.org/10.1007/BF00581430