[Functional expression of calcium channels in reconstitution models].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Nargeot.
Explore the source record for details and available documents.
Voltage-gated calcium channels are involved in a large variety of cellular functions such as excitation-contraction coupling, hormone secretion, firing and pacemaker activity, gene activation and proliferation. Cloning of complementary DNAs encoding for calcium channel subunits has challenged the study of the functional properties of calcium channels and has allowed analysis of the molecular basis of calcium channel diversity. Recently, pore-forming subunits of T-type calcium channels have been cloned. Recent data describing the genes encoding calcium channels, their molecular and pharmacological studies, as well as their linkage to human genetic diseases are reviewed in this article.
Voltage clamp experiments have been conducted on frog atrial fibers to study the mechanism of the negative inotropic effect induced by muscarinic agonists. The results have shown that muscarinic agonists exert a dual effect: 1.) A reduction of the slow inward current (Is) amplitude; 2.) An increase in the potassium conductance. Dose-effect curves for both Is and K+ extra-current show that the inhibition of Is appears at lower agonist concentrations and can mainly account for the negative inotropic effect. It is suggested that the action of muscarinic agonists may involve one or two types of muscarinic receptors. The slow channel conductance could be controlled by the intracellular cyclic nucleotides concentration (cAMP and cGMP) via a muscarinic receptor (R1) with a high affinity for agonists. The increase in the potassium conductance could be mediated either by an increase in the intracellular free Ca2+ concentration or by a second type of muscarinic receptor (R2) with a lower affinity for muscarinic agonists and controlling a specific potassium channel.