Effects of taurine deficiency on arrhythmogenesis and excitation-contraction coupling in cardiac tissue.

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Taurine is the major constituent of the free amino acid pool of mammalian myocardium, but its precise function is little understood. There is little biosynthesis of taurine within the heart; instead its mM levels are determined by active transmembrane transport by a specific carrier. It is not found in proteins, neither is it a substrate for metabolism. Taurine deficiency, however, produces cardiac electrophysiological and mechanical abnormalities (Lake et al., 1987; 1990) and life-threatening dilated cardiomyopathy documented by echocardiography in cats and foxes (Pion et al., 1987; Moise et al., 1989). Novotny et al. (1991) have recently described deficits in left ventricular systolic pressure development in such cats. Taurine supplements can reverse these conditions, and are also beneficial in the treatment of human congestive heart failure of many etiologies (Azuma et al., 1985) and a rabbit model of this condition (Azuma et al., 1984). The sites of action of most of these effects are unknown. The majority of studies have described the pharmacological effects of exogenous taurine in doses which far exceed the micromolar levels normally found in the plasma. Interactions with calcium (Ca) are suggested by the observations that taurine administration has positive inotropic effects (Huxtable, 1976), prevents Ca paradox (Kramer et al., 1981) and delays the onset of Ca accumulation which causes necrotic lesions in genetic cardiomyopathic hamsters (McBroom and Welty, 1977).