ArticleThe Journal of physiology2002
Voltage-dependent inactivation of L-type Ca2+ currents in guinea-pig ventricular myocytes.
Article in The Journal of physiology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Phosphoinositide Depletion and Compensatory Phospho-Signaling in Angiotensin II-Induced Heart Disease.Circulation research · 2026Article
- L-type channel inactivation balances the increased peak calcium current due to absence of Rad in cardiomyocytes.The Journal of general physiology · 2021Article
- Interplay of voltage and Ca-dependent inactivation of L-type Ca current.Progress in biophysics and molecular biology · 2010Review
- Enhanced L-type calcium currents in cardiomyocytes from transgenic rats overexpressing SERCA2a.Experimental and clinical cardiology · 2010Article
- Accelerated inactivation of cardiac L-type calcium channels triggered by anaesthetic-induced preconditioning.British journal of pharmacology · 2009Article
- Kinetic properties of the cardiac L-type Ca2+ channel and its role in myocyte electrophysiology: a theoretical investigation.Biophysical journal · 2007Article
- FPL 64176 modification of Ca(V)1.2 L-type calcium channels: dissociation of effects on ionic current and gating current.Biophysical journal · 2005Article
- Ionic currents involved in shock-induced nonlinear changes in transmembrane potential responses of single cardiac cells.Pflugers Archiv : European journal of physiology · 2004Article
- Physiological modulation of inactivation in L-type Ca2+ channels: one switch.The Journal of physiology · 2004Review
- Functional roles of cytoplasmic loops and pore lining transmembrane helices in the voltage-dependent inactivation of HVA calcium channels.The Journal of physiology · 2004Review
- Modulation of inactivation of cardiac L-type Ca2+ channels.The Journal of physiology · 2002Article
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1 author at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to describe the kinetics of voltage-dependent inactivation of native cardiac L-type Ca(2+) currents. Whole-cell currents were recorded from guinea-pig isolated ventricular myocytes. Voltage-dependent inactivation was separated from Ca(2+)-dependent inactivation by replacing extracellular Ca(2+) with Mg(2+) and recording outward currents through Ca(2+) 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 tau(f) approximately equal 30 ms and tau(s) approximately equal 300 ms, the fast component of decay accounted for 70 % of the current amplitude. In basal conditions Ca(2+) current availability was sigmoid. Isoproterenol (isoprenaline) evoked a large increase in a time-independent component of the Ca(2+) current which also increased with depolarisation. This was responsible for the apparent recovery of Ca(2+) 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 Ca(2+) channels to membrane voltage. In basal conditions, voltage accelerated inactivation. In isoproterenol, voltage could also reduce inactivation.
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