Pflugers archiv-european journal of physiology vol:441 issue:1 pages:39-48
Sodium ions have been reported to alter the permeation properties of L- and N-type Ca2+ channels. Here in frog atrial cardiomyocytes under whole-cell patch-clamp conditions, we have examined the effects of lowering the external Na+ concentration on the amplitude of T-type Ca2+ current, I-CaT, and on the relief of its steady-state inactivation by large depolarizing prepulses, I-CaT facilitation. A partial reduction in Na+ ion concentration did not significantly alter I-CaT amplitude elicited at -50 mV. However, after a large depolarization, low-Na+ solutions enhanced the relief of inactivation and induced I-CaT facilitation. This facilitation occurred independently of the divalent charge carrier, high intracellular Ca2+ buffering or the intracellular Na+ content. Its effects were additional to the beta -adrenergic effects mediated by a decrease of G(i/o)-protein inhibitory tone. In Ca2+-free solution the very large T-type current, then carried by Na+ ions, showed only a weak relief of inactivation. In conclusion, I-CaT facilitation - which, as previously reported, is modulated by the transient voltage-dependent relief of G(i)-protein inhibitory tone - is further enhanced in a low-Na+ solution. In Ca2+-free solution, relief of inactivation due to re-openings dependent on the divalent charge carrier is improbable. It thus appears that for a short while after a large depolarization, external Na+ compete with Ca2+ ions on permeation-controlling sites, so as to modulate channel re-openings and thus the amplitude of voltage-facilitated I-CaT independently of the control exerted by the inhibitory G-protein.