Interdependence of intracellular taurine and sodium in guinea pig heart

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Abstract
Objective: The aim was to investigate the effects of raising intracellular taurine on the intracellular sodium activity (aNai) in isolated guinea pig ventricular myocytes, and the effect of procedures that raise intracellular sodium on taurine concentration in the perfused guinea pig ventricular tissue. Methods: Taurine was introduced into the sarcoplasm of isolated ventricular myocytes, either during cell isolation or by diffusion from a penetrating micropipette, and the effect on aNai was measured using an ion sensitive microelectrode. Guinea pig hearts, mounted on a Langendorff apparatus, were perfused with a variety of physiological media and the level of taurine in the ventricles determined using high pressure liquid chromatography. Results: An increase in intracellular taurine caused by its presence during cell isolation or by diffusion from a micropipette significantly reduced the aNai of isolated myocytes at rest, during perfusion with Ca depleted solutions, or on inhibition of the Na pump. In the guinea pig ventricles, taurine at 13.0(SEM 0.6) mmol·kg−1 wet weight comprised up to 45% of the free amino acids; since plasma taurine was 64(13) μmol·litre−1, this means that in vivo a large outwardly directed gradient for taurine exists (equivalent to a free energy of 13.7 KJ·mol−1). Upon perfusion with Ca,Mg free Tyrode solution (which raises intracellular sodium markedly), a time dependent loss of taurine occurred. Both the rate of loss and the total amount lost were increased when the Na pump was also inhibited. This loss of tissue taurine was not due to release from dead or lysed cells, as it was antagonised by procedures known to reduce the rise of aNai during Ca depletion, was inhibited by β alanine (an inhibitor of taurine transport), and the fall in tissue taurine was not correlated with the appearance of lactate dehydrogenase in the effluent. Conclusions: The data from isolated myocytes and perfused guinea pig hearts were consistent with the presence of a Na/taurine symport which is activated to cause efflux of Na and taurine when either rise above their physiological level. Cardiovascular Research 1992;26:897–905

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