Taurine, an ubiquitous amino acid in the animal kingdom was found widely throughout the body and particularly in high concentrations in excitable tissues. Despite its prevalence no specific physiological function was ascribed to taurine in mammals aside from its well characterized role in bile salt formation in some species. Evidence implied that taurine served a homeostatic function in excitable tissues such as nerve and muscle by stabilizing membranes in these tissues through the regulation of cell membrane permeability to ions. Taurine influenced K+, Cl- and Ca2+ translocation in nerve, skeletal muscle and heart. It mitigated drug-induced abnormalities in the ECG of the heart and was found in higher than normal amounts in states of cardiovascular pathology, i.e., congestive heart failure and hypertension in man, spontaneous and stress-induced hypertension in rats and cardiac hypertrophy in dogs and rats. Because of the lack of information concerning the metabolism of taurine by the heart and the inability of investigators to modify cardiac taurine levels in vivo, no cause and effect relationship was yet been proposed between altered cardiac taurine levels and naturally occurring states of cardiac pathology.