PMID: 8974043Oct 1, 1996Paper

Regulation of the slow Ca++ channels of myocardial cells

Molecular and Cellular Biochemistry
N SperelakisK Sumii

Abstract

Contraction of the heart is regulated by a number of mechanisms, such as neurotransmitters, hormones, autacoids, pH, intracellular ATP, and Ca++ ions. These actions are mediated, at least in part, by actions on the sarcolemmal slow (L-type) Ca++ channels, exerted directly or indirectly. The major mechanisms for the regulation of the slow Ca++ channels of myocardial cells includes the following. cAMP/PK-A phosphorylation stimulates the slow Ca++ channel activity, whereas cGMP/PK-G phosphorylation inhibits. DAG/PK-C phosphorylation and tyrosine kinase phosphorylation are suggested to stimulate the slow Ca++ channel activity. Intracellular application of Gs alpha protein increases the slow Ca++ currents (ICa(L)). Lowering of intracellular ATP inhibits ICa(L). Acidosis and increase in [Ca]i inhibits ICa(L). A number of changes in the Ca++ channels also occur during development and aging. Thus, it appears that the slow Ca++ channel is a complex structure, including perhaps several associated regulatory proteins, which can be regulated by a number of extrinsic and intrinsic factors, and thereby control can be exercised over the force of contraction of the heart.

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Citations

Feb 27, 2010·Pflügers Archiv : European journal of physiology·András Varró, István Baczkó
Jul 4, 1998·Zygote : the Biology of Gametes and Early Embryos·H Ouadid-Ahidouch
Mar 11, 2000·British Journal of Pharmacology·I M FearonC Peers
Nov 20, 1998·Research in Experimental Medicine. Zeitschrift Für Die Gesamte Experimentelle Medizin Einschliesslich Experimenteller Chirurgie·L YanH R Weiss
Dec 4, 2003·Biochimica Et Biophysica Acta·Elena A LukyanetzPlaton G Kostyuk
Aug 8, 1997·Biochemical and Biophysical Research Communications·R G O'NeilN J Karin
Jun 8, 2004·Journal of Applied Physiology·Cherry Ballard-CroftJureta W Horton

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