Abstract
Objective: Many amino acids have been shown to be cotransported with Na+ in a variety of tissues but evidence for an Na+ dependent efflux in the heart is restricted to taurine. The aim of this study was to determine the intracellular levels of the principal amino acids, alanine, glutamine, glutamate, and aspartate, when the heart was beating at normal or low temperature, during exposure to strophanthidin, and when the heart was arrested with either Ca2+, Mg2+-free Tyrode solution (a condition known to raise intracellular Na+) or with a high K+ Tyrode solution. Methods: Guinea pig hearts, mounted on a Langendorff apparatus, were perfused with a variety of media and the level of amino acids in the ventricles determined using high performance liquid chromatography. Results: During perfusion with normal Tyrode solution a time dependent fall in tissue glutamine, glutamate, and aspartate, but not alanine, was observed. Exposure of the beating heart to strophanthidin (0.2 mM) or cooling to 20°C, which should induce a similar increase in [Na+]i but have opposite effects on metabolism, had different effects on tissue amino acids. Cooling did not affect the level of amino acids whereas strophanthidin produced an effect consistent with an activation of a glutamate-alanine aminotransferase. Arresting the heart with Ca2+, Mg2+-free Tyrode solution provoked a marked fall in all amino acids which was associated with their appearance in the effluent. This loss of the amino acids was antagonised by conditions known to reduce the rise in intracellular Na+ concentration and increased by inhibition of the Na+ pump. Comparison of the beating heart with the heart arrested with high K+ Tyrode solution showed no difference in the levels of glutamate or aspartate, with a small fall in alanine and taurine and raised glutamine. Conclusions: The data from beating or arrested hearts are consistent with the presence of amino acid/Na+ cotransport systems but the levels of amino acids free in the sarcoplasm depend on an interaction between amino acid transport driven by the changes in the Na+gradient and the effects of metabolism. Cardiovascular Research 1993;27:1810-1814

This publication has 0 references indexed in Scilit: