Ventricular action potential and L-type calcium channel in infarct-induced hypertrophy in rats.

The present investigation was aimed at characterization of: (1) action potential parameters; and (2) L-type calcium channels in the hypertrophied ventricular tissue surviving an extensive healed myocardial infarction in the rat. Myocardial infarction was produced in Wistar rats by ligation of the left coronary artery. One to 2 months later, their hearts were subjected to electrophysiologic study. The main difference in subendocardial transmembrane potentials recorded with intracellular microelectrodes was an increase in action potential duration (APD). In the left ventricle, the infarcted/sham-operated APD ratio ranged from 2.7 to 7.2, whereas in the right ventricle it ranged from 1.6 to 2.3 in different regions. When compared with control cells, ventricular myocytes from infarcted hearts were found to be larger (P < 0.01) and showed a reduction (P < 0.05) in L-type calcium current (LCa,L) density obtained by whole cell, patch clamp (at 0 mV: 4.44 +/- 0.41 in infarcted vs 8.03 +/- 1.22 pA/pF in normal). The time course of decay of the currents could be fitted by two exponential functions in both normal and infarcted hearts. There was a tendency toward an increase in the time constant of the slower component of inactivation, tau 2, significant only at +20 mV (215 +/- 25 vs 151 +/- 15 msec). Cardiac hypertrophy of healed infarction in rats is associated with lengthening of the action potential in both ventricles. The main alteration observed in ICa,L was a decrease in the current density. Thus, alteration of the calcium channel is not the determinant factor of APD increase.