title: Ontogenesis of transmembrane signaling systems for control of cardiac Ca2+ channels.
abstract: Cardiac ICa is primarily controlled by the Ca2+ influx across the cell membrane during the action potential. Neurotransmitters and hormones are known to play an important role in controlling the availability of cardiac Ca2+ slow channels and [Ca]i through the transmembrane signaling systems, such as the receptor-adenylate cyclase system and the PI hydrolysis system. This article has reviewed some of the important properties of the transmembrane signaling systems for the control of Ca2+ channels and how they changed during development, especially in the rat heart. Since the phosphorylation hypothesis was first proposed over 15 years ago, considerable advances have been made in understanding the mechanisms for regulation of Ca2+ slow channels at the molecular level. During development, the properties of the cardiac Ca2+ channels, as well as the transmembrane signaling systems, change electrophysiologically, pharmacologically, and biochemically. Because conflicting data have been reported on the developmental changes in these properties, it is still not clear how the complex physiological function of the Ca2+ channels is gradually integrated during development. To answer this question, more data, new concepts, and new approaches are required.
authors.affiliation: Department of Physiology and Biophysics, College of Medicine, University of Cincinnati, Ohio 45267.
authors.forename: M
authors.initials: M
authors.lastname: Kojima
authors.forename: N
authors.initials: N
authors.lastname: Sperelakis
authors.forename: H
authors.initials: H
authors.lastname: Sada
mesh_terms: D000375:Aging / Q000502:physiology*; D000818:Animals; D002118:Calcium / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D004361:Drug Tolerance / Q000502:physiology; D006321:Heart / Q000254:growth & development* / Q000294:innervation; D008564:Membrane Potentials; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism*; D009638:Norepinephrine / Q000378:metabolism; D010042:Ouabain / Q000494:pharmacology; D051381:Rats; D015398:Signal Transduction; D000254:Sodium-Potassium-Exchanging ATPase / Q000187:drug effects
chemical_list: D015220:Calcium Channels; D010042:Ouabain; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium; D009638:Norepinephrine