ArticleThe Journal of physiology2002
Beta-adrenergic and muscarinic agonists modulate inactivation of L-type Ca2+ channel 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 9 papers.
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Who cites it
9 citing papers in PubMed, 18 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
- Verrucotoxin, a stonefish venom, modulates calcium channel activity in guinea-pig ventricular myocytes.British journal of pharmacology · 2007Article
- Calsequestrin mutation and catecholaminergic polymorphic ventricular tachycardia: a simulation study of cellular mechanism.Cardiovascular research · 2007Article
- Kinetic properties of the cardiac L-type Ca2+ channel and its role in myocyte electrophysiology: a theoretical investigation.Biophysical journal · 2007Article
- Ionic mechanisms of cardiac cell swelling induced by blocking Na+/K+ pump as revealed by experiments and simulation.The Journal of general physiology · 2006Article
- 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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The objective of this study was to examine the effects of isoproterenol (isoprenaline) and carbachol upon voltage-dependent inactivation of L-type Ca(2+) current (I(Ca,L)). I(Ca,L) was recorded in guinea-pig isolated ventricular myocytes in the presence and absence of extracellular Ca(2+) to separate total inactivation and voltage-dependent inactivation. In the presence of Ca(2+), isoproterenol and carbachol had 'competitive' effects upon the relationships between membrane voltage and I(Ca,L) amplitude and inactivation. Neither agonist had a marked effect upon the decay of inward I(Ca,L) carried by Ca(2+). In the absence of Ca(2+), isoproterenol severely reduced and slowed I(Ca,L) inactivation; this effect was reversed by carbachol. Under control conditions decay was dominated by fast inactivation. Isoproterenol reduced fast-inactivating and increased time-independent currents in a dose-dependent manner. These effects were counteracted by carbachol. There was a reciprocal relationship between the amplitude of fast-inactivating and time-independent currents with agonist stimulation. It is concluded that agonist modulation of rapid voltage-dependent inactivation of L-type Ca(2+) channels involves an 'on-off' switch.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.