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Received February 27, 2002
Accepted after revision April 2, 2002
1 CNRS UMR 6542, Faculté des Sciences, Parc de Grandmont, 37200 TOURS, France
* To whom correspondence should be addressed. E-mail: findlay{at}univ-tours.fr.
The objective of this study was to examine the effect of ß-adrenergic stimulation upon voltage- and Ca2+-induced inactivation of native cardiac L-type Ca2+ channels. Whole-cell currents were recorded from guinea-pig isolated ventricular myocytes. Total and voltage-dependent inactivation was separated by replacing extracellular Ca2+ with Mg2+. L-type Ca2+ channel behaviour was monitored with outward Ca2+ channel currents. First, the voltage dependence of inactivation was studied at fixed times (50 and 1000 ms) after activation. This showed that under control conditions Ca2+ contributed little to inactivation. In isoproterenol (isoprenaline), voltage-dependent inactivation was markedly reduced and Ca2+ contributed largely to total inactivation. Second, the time dependence of inactivation was studied at a fixed voltage (+10 mV). In control conditions the fast phase of inactivation (
f ~15 ms) was reduced to the same extent by ryanodine (f ~30 ms) and the absence of Ca2+ (f ~30 ms) while the slow phase of inactivation (s ~70 ms) was reduced by ryanodine (s ~160 ms) and further reduced in the absence of Ca2+ (s ~300 ms). In isoproterenol, biphasic inactivation of Ca2+ currents (f ~4 ms, s ~60 ms) was replaced by a single slow ( ~450 ms) phase of inactivation in the absence of Ca2+. It is concluded that, under control conditions Ca2+ channel current decay is largely dominated by rapid voltage-dependent inactivation, while in isoproterenol this is replaced by Ca2+-induced inactivation.
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