Conservation of L-type Ca2+ current characteristics in endo- and epicardial myocytes from rat left ventricle with pressure-induced hypertrophy.

Cardiac hypertrophy alters the regional distribution of action potential duration by affecting the magnitude and kinetics of underlying ionic currents. In the present study, the effect of pressure-induced cardiac hypertrophy on the magnitude and kinetics of the L-type Ca2+ current ( I(CaL)) was investigated in endo- and epicardial myocytes of the rat left ventricular free wall. Cardiac hypertrophy was induced by stenosis of the ascending aorta (AS), which led to a pressure difference between the left ventricular peak pressure and the peripheral systolic blood pressure of 84+/-6 mmHg ( n=5, P<0.0001). Sham-operated animals served as controls ( n=7). I(CaL) was investigated using the whole-cell patch-clamp technique. The magnitude of I(CaL) as well as its inactivation, steady-state activation, steady-state inactivation and recovery from inactivation were similar in endo- and epicardial myocytes of sham-operated rats. In myocytes isolated from AS animals, I(CaL) magnitude was significantly greater than in sham-operated animals (2407+/-127 pA, n=42 versus 1904+/-102 pA, n=33; P<0.01). This difference disappeared, however, when I(CaL) was normalized to cell capacitance. The kinetic properties of I(CaL) were unaffected by AS in both endo- and epicardial myocytes. In conclusion, in pressure-induced cardiac hypertrophy the density and kinetics of I(CaL) are preserved. This suggests that an additional insertion or recruitment of channels normally underlying I(CaL) into the cell membrane compensates for the increased cell size associated with hypertrophy.