Electrophysiological effects of homocysteine in isolated rat right ventricular papillary muscles and left atria.
There is clinical and epidemiological evidence that elevated plasma homocysteine (Hcy) levels are associated with increased myocardial infarction mortality; however, very little is known about Hcy's direct cardiac effects. Thus, we aimed to characterize the cellular electrophysiologic effects of Hcy, a sulfur-containing amino acid in isolated rat hearts. A conventional microelectrode technique was used in left atria and right ventricular papillary muscles. At concentrations higher than 10(6) M, Hcy significantly decreased the maximum rate of rise of the depolarization phase (Vmax) in both cardiac preparations in a dose-dependent manner. Hcy at 10(-4)-5 x 10(-4) M concentrations increased the action potential duration (APD) at late stages of repolarization (at 75% and 90% of APD) both in atria and in ventricles. There was a slight decrease in action potential amplitude in ventricular papillary muscles and atria at concentrations higher that 10(-5) M. The resting membrane potential and the early repolarization phase (APD25 and APD50) remained unchanged in every preparation studied at all concentrations of Hcy administered. The present data suggest that homocysteine may decrease the Na+ channel activity in in vitro cardiac preparations. reserved.
D000200:Action Potentials / Q000187:drug effects*; D000818:Animals; D016279:Atrial Function, Left / Q000187:drug effects; D006321:Heart / Q000187:drug effects*; D006710:Homocysteine / Q000494:pharmacology*; D008297:Male; D010210:Papillary Muscles / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D015222:Sodium Channels / Q000187:drug effects; D016278:Ventricular Function, Right / Q000187:drug effects