NDLI: Dihydropyridine-sensitive Ca2+ channels in mammalian skeletal muscle cells in culture: electrophysiological properties and interactions with Ca2+ channel activator (Bay K8644) and inhibitor (PN 200-110).

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Dihydropyridine-sensitive Ca2+ channels in mammalian skeletal muscle cells in culture: electrophysiological properties and interactions with Ca2+ channel activator (Bay K8644) and inhibitor (PN 200-110).

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Dihydropyridine-sensitive Ca2+ channels in mammalian skeletal muscle cells in culture: electrophysiological properties and interactions with Ca2+ channel activator (Bay K8644) and inhibitor (PN 200-110).

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Cognard, C. Fosset, M. Galizzi, J. P. Romey, G. Lazdunski, M.
Abstract	The whole-cell patch-clamp technique has been used to analyze the properties of the dihydropyridine-sensitive Ca2+ channel in rat skeletal muscle cells (myoballs) in culture. The potential dependence of Ca2+-channel activation is similar to that observed in cardiac cells. However, the skeletal muscle Ca2+ channel is activated more slowly (by a factor of about 10). The voltage dependence of Ca2+-channel inactivation indicates a half-maximal inactivation (Vh0.5) at -72 mV as compared to Vh0.5 = -35 mV for cardiac cells. Blockade of the skeletal muscle Ca2+ channel by the dihydropyridine (+)-PN 200-110 is voltage dependent, with a half-maximal effect (K0.5) of 13 nM for an application of the drug to the myoball membrane held at -90 mV and of 0.15 nM for an application at a potential of -65 mV. The 100-fold difference in apparent affinity is interpreted as a preferential association of PN 200-110 with the inactivated form of the Ca2+ channel. The K0.5 value found from electrophysiological experiments for the binding to the inactivated state (K0.5 = 0.15 nM) is nearly identical to the equilibrium dissociation constant found from binding experiments with (+)-[3H]PN 200-110 using transverse-tubular membranes (Kd = 0.22 nM). The dihydropyridine activator Bay K8644 acts by increasing Ca2+ current amplitude and by slowing down deactivation.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	5
Volume Number	83
Language	English
Publisher	National Academy of Sciences
Publisher Date	1986-04-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Ion Channels Physiology Muscles Nifedipine Analogs & Derivatives Oxadiazoles Pharmacology Action Potentials Drug Effects Animals Cells, Cultured Electric Conductivity Isradipine Membrane Potentials Cytology Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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