Role of intracellular taurine in monensin-induced Na+, Ca++ accumulation and mechanical dysfunction in isolated rat hearts

ABSTRACT

It has been postulated that the intracellular taurine is co-transported with Na+ down a concentration gradient and prevents the intracellular accumulation of sodium. It is therefore, expected that an elevated level of intracellular taurine prevents the sodium-promoted calcium influx to protect the cellular damages associated with sodium and calcium overload. In the present study, we evaluated the effects of intra- and extracellular taurine on the myocardial Na+ and Ca++ contents and the cardiac functions in isolated rat hearts which were loaded with sodium by monensin, a Na+/-ionophore. Monensin caused a dose-dependent increase in intracellular Na+ accompanied with a subsequent increase in intracellular Ca++ and a mechanical dysfunction. In this monensin-treated heart, myocardial taurine content was decreased with a concomitant increase in the release of taurine. The monensin-induced increases in intracellular Na+, Ca++ and depression of cardiac function were prevented in the hearts of which taurine content had been increased by high-taurine diet. Conversely, in the hearts of which taurine concentration gradient had been decreased by addition of taurine in the perfusate, the monensin-induced increases in Na+, Ca++ and functional depression were accelerated. These results suggest that taurine, depending on the intra-extracellular concentration gradient, can affect intracellular sodium and calcium concentrations, and that an increased intracellular taurine may play a role in protection of myocardial dysfunction associated with the sodium and calcium overload.