Perfusion of rat hearts with buffer containing 300 microM L-methionine led to a decrease in Ca(2+)-induced Ca2+ release in sarcoplasmic reticulum (SR) but an increase in calcium-independent Ca2+ release from junctional SR. These effects of L-methionine were not altered by exposure of the hearts to high levels of extracellular taurine, but changes in the size of the intracellular taurine pool appear to modulate calcium transport in SR through two mechanisms. First, millimolar concentrations of taurine can directly promote release of calcium from 45Ca(2+)-loaded junctional SR vesicles. Second, taurine serves as an inhibitor of SR phospholipid methyltransferase, an enzyme that appears to be responsible for methionine-mediated loss in Ca(2+)-induced Ca2+ release activity and promotion of Ca(2+)-independent Ca2+ release. The data imply that modulation of the intracellular taurine pool may affect cellular calcium homeostasis and myocardial contractile function. This may be important in development of the cardiomyopathy linked to taurine deficiency.