Basic Residues in the C-Terminal Region of Troponin T are Critical in Skeletal Muscle Regulation

Abstract

I Na,late could not be converted to an ''increasing'' morphology by application of isoproterenol, calmodulin, AP-like ramp voltage command or command APs recorded from guinea pig cells. Conventional voltage clamp experiments revealed that the ''increasing'' I Na,late profile in guinea pig is determined by the slow decay of I Na,late in this species. I Na,late was increased by isoproterenol but not by calmodulin in canine myocytes. When APs were recorded from multicellular ventricular preparations with sharp microelectrode, tetrodotoxin decreased AP duration in a reverse rate-dependent manner, which effect was the largest in human, while smaller in canine and the smallest in guinea pig preparations. The shape of I Na,late under the AP is likely determined by the different inactivation kinetics of the sodium channels that generate I Na,late . Variances between different species in the actual sodium channel subtypes that contribute to I Na,late might underlie the differences observed in the macroscopic current. Canine myocytes seems to be the best model of human ventricular cells regarding I Na,late .