NDLI: Long-chain fatty acids activate calcium channels in ventricular myocytes.

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Long-chain fatty acids activate calcium channels in ventricular myocytes.

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Long-chain fatty acids activate calcium channels in ventricular myocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Huang, J. M. Xian, H. Bacaner, M.
Description	Author Affiliation: Huang JM ( Department of Physiology, University of Minnesota, Minneapolis 55455.);
Abstract	Nonesterified fatty acids accumulate at sites of tissue injury and necrosis. In cardiac tissue the concentrations of oleic acid, arachidonic acid, leukotrienes, and other fatty acids increase greatly during ischemia due to receptor or nonreceptor-mediated activation of phospholipases and/or diminished reacylation. In ischemic myocardium, the time course of increase in fatty acids and tissue calcium closely parallels irreversible cardiac damage. We postulated that fatty acids released from membrane phospholipids may be involved in the increase of intracellular calcium. We report here that low concentrations (3-30 microM) of each long-chain unsaturated (oleic, linoleic, linolenic, and arachidonic) and saturated (palmitic, stearic, and arachidic) fatty acid tested induced multifold increases in voltage-dependent calcium currents (ICa) in cardiac myocytes. In contrast, neither short-chain fatty acids (less than 12 carbons) or fatty acid esters (oleic and palmitic methyl esters) had any effect on ICa, indicating that activation of calcium channels depended on chain length and required a free carboxyl group. Inhibition of protein kinases C and A, G proteins, eicosanoid production, or nonenzymatic oxidation did not block the fatty acid-induced increase in ICa. Thus, long-chain fatty acids appear to directly activate ICa, possibly by acting at some lipid sites near the channels or directly on the channel protein itself. We suggest that the combined effects of fatty acids released during ischemia on ICa may contribute to ischemia-induced pathogenic events on the heart that involve calcium, such as arrhythmias, conduction disturbances, and myocardial damage due to cytotoxic calcium overload.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	14
Volume Number	89
Language	English
Publisher	National Academy of Sciences
Publisher Date	1992-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Calcium Channels Physiology Fatty Acids Pharmacology Heart Ion Channel Gating Drug Effects Animals Arachidonic Acid Cells, Cultured Electric Conductivity Chemistry GTP-Binding Proteins Guinea Pigs In Vitro Techniques Myocardium Cytology Protein Kinase C Antagonists & Inhibitors Protein Kinase Inhibitors Structure-Activity Relationship Time Factors Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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