Modulation of Myocardial Contractility by Taurine: Absence of its Interactions with the Effects of Low [CA2+]0, Verapamil, Bay K 8644, and α - and β-Adrenoceptor Agonists in the Rabbit Papillary Muscle

摘要: Since taurine is by far the most abundant sulfur-containing amino acid in mammalian myocardium [1–3], its role regulation of myocardial contractility physiological and pathophysiological conditions has been intensively pursued. The biochemical aspects transport mechanism—including changes content resulting from modification uptake into leakage cells (e.g., β-adrenoceptor stimulation [4–6]), pharmacological guanidinoethyl sulfonate, or β-alanine [7,8]), congestive heart failure [9–12], ischemia [13–15], hypoxia [16]) interventions—have quite well documented (for review, see [1]). In contrast, functional remains relatively unclear spite continuous research interest extensive effort to elucidate subcellular mechanism that involved [17].