title: Direct regulation of cardiac Ca2+ channels by G proteins: neither proven nor necessary?
abstract: The cardiac L-type Ca2+ channel has served as a model for ion channel regulation for over a decade. The Ca2+ current is increased by beta-adrenoceptor stimulation and this effect is inhibited by muscarinic acetylcholine receptor stimulation. It is well established that beta-adrenoceptor stimulation increases this current largely by cAMP-dependent phosphorylation but recently data have been presented that suggest that this channel may also be regulated directly by G proteins. This review by Criss Hartzell and Rodolphe Fischmeister evaluates evidence for this second regulatory pathway and concludes that, although G proteins affect cardiac Ca2+ channels in bilayers and excised patches, there is little evidence that this pathway is physiologically significant.
authors.affiliation: Department of Anatomy and Cell Biology, Emory University School of Medicine, Atlanta, GA 30322.
authors.forename: H C
authors.initials: HC
authors.lastname: Hartzell
authors.forename: R
authors.initials: R
authors.lastname: Fischmeister
mesh_terms: D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000818:Animals; D015220:Calcium Channels / Q000187:drug effects / Q000502:physiology*; D019204:GTP-Binding Proteins / Q000502:physiology*; D006321:Heart / Q000187:drug effects / Q000502:physiology*; D006801:Humans; D009200:Myocardial Contraction; D010766:Phosphorylation
chemical_list: D000318:Adrenergic beta-Agonists; D015220:Calcium Channels; D001498:3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethyl-5-nitro-4-(2-(trifluoromethyl)phenyl)-, Methyl ester; D019204:GTP-Binding Proteins