[The calcium channel: electrophysiological findings in cardiac cells].
General properties of the calcium channel are analyzed in the myocardium under voltage clamp conditions both in multicellular properties and in single isolated cells. More recently the patch-clamp has allowed us to study single channels. In normal conditions, the selectivity of the calcium channel to Ca2+ ions is very high; however, in the absence of calcium many divalent cations and even Na ions can go through this channel. Kinetic analysis shows: calcium channel inactivation depends on Ca2+ entry rather than on membrane potential, opening of this channel requires at least two transitions of closed states before the open state. Many works refer to pharmacology of the calcium channel in heart tissue. beta-adrenergic stimulation induces a large increase in current amplitude related to the increase in maximal conductance without variation in the unitary conductance. Two interpretations are available: an increase in the opening probability and/or an increase in the number of available channels, both are consecutives to phosphorylations of the channel. Cholinergic stimulation seems to have little effect. Studies of calcium antagonists have revealed that all these substances have, at various levels, use-dependent and voltage-dependent inhibitory effect. Moreover, some dihydropyridine derivatives can even, activate the channel. Antiarrhythmic as well as general anaesthetic agents have an inhibitory action on the calcium channel besides their effects on the sodium channel or the Na-Ca exchange. Very recently, the existence of another calcium conductance was demonstrated. It is characterized by a low threshold, a pure voltage-dependent inactivation, a relatively weak sensitivity to anticalcic agents and neurotransmettors.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004594:Electrophysiology; D007473:Ion Channels / Q000502:physiology*; D009206:Myocardium / Q000378:metabolism*
D007473:Ion Channels; D002118:Calcium
Canal calcium: données électrophysiologiques dans les cellules cardiaques.