Effects of chronic intermittent hypobaric hypoxia on the L-type calcium current in rat ventricular myocytes.

This study was conducted to investigate the role of the L-type calcium channel in the cardioprotection afforded by chronic intermittent hypobaric hypoxia (CIHH). Rats were exposed to CIHH for 28 days (CIHH28) or 42 days (CIHH42), respectively, before their ventricular myocytes were isolated for electrophysiological studies. Under normal recording conditions, no difference was found in the current density and voltage dependence of activation and inactivation of I(caL) recorded in CIHH28 and CIHH42 myocytes, compared with those in control myocytes isolated from rats exposed to sea-level air. Under simulated ischemic (I) conditions, the peak I(ca.L) decreased in all groups. However, the decreases of I(caL) in CIHH rats were of a lesser extent than those in the control. Simulated ischemia also induced an approximately 10-mV positive shift of the steady-state inactivation curve of I(caL) in control but not in CIHH myocytes, as measured by the half-maximal inactivation potentials (V(1/2)). The results suggest that adaptation to CIHH might have increased the tolerability of cardiac myocytes to ischemic challenges through preventing electrophysiological remodeling of the calcium channel.