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J Physiol Volume 545, Number 2, 389-397, December 1, 2002 DOI: 10.1113/jphysiol.2002.029637
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Journal of Physiology (2002), 545.2, pp. 389-397
© Copyright 2002 The Physiological Society
DOI: 10.1113/jphysiol.2002.029637

Voltage-dependent inactivation of L-type Ca2+ currents in guinea-pig ventricular myocytes

Ian Findlay

CNRS UMR 6542, Faculté des Sciences, Université de Tours, France

The objective of this study was to describe the kinetics of voltage-dependent inactivation of native cardiac L-type Ca2+ currents. Whole-cell currents were recorded from guinea-pig isolated ventricular myocytes. Voltage-dependent inactivation was separated from Ca2+-dependent inactivation by replacing extracellular Ca2+ with Mg2+ and recording outward currents through Ca2+ channels. Voltage-dependent inactivation accelerated from slow monophasic decay at -30 mV to maximal rapid biphasic decay at +20 mV. Maximal voltage-dependent inactivation occurred with tauf ~30 ms and taus ~300 ms, the fast component of decay accounted for 70 % of the current amplitude. In basal conditions Ca2+ current availability was sigmoid. Isoproterenol (isoprenaline) evoked a large increase in a time-independent component of the Ca2+ current which also increased with depolarisation. This was responsible for the apparent recovery of Ca2+ channel current availability at positive membrane potentials and thus a U-shaped availability-voltage (A-V) relationship. It is concluded that beta-adrenergic stimulation altered the reaction of native cardiac L-type Ca2+ channels to membrane voltage. In basal conditions, voltage accelerated inactivation. In isoproterenol, voltage could also reduce inactivation.



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