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Arachidonic Acid Inhibition of Muscarinic Receptor-Mediated Nitric Oxide Production Occurs at the Level of Calcium Mobilization in Chinese Hamster Ovary Cells

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Arachidonic Acid Inhibition of Muscarinic Receptor-Mediated Nitric Oxide Production Occurs at the Level of Calcium Mobilization in Chinese Hamster Ovary Cells

Content Provider	Springer Nature Link
Author	Linden, David R. El Fakahany, Esam E.
Copyright Year	2002
Abstract	Strong evidence supports that nitric oxide (NO) alters cell signaling pathways involving arachidonic acid (AA). Little is known, however, about the reciprocal modulation of nitrergic pathways by AA. The effects of exogenous AA on signal transduction of M$_{1}$ muscarinic acetylcholine receptors were investigated in a model system of stably transfected Chinese hamster ovary cells. AA concentration-dependently inhibited the effects of carbachol in producing NO (IC$_{50}$ = 191 μM) but did not alter inositol phosphate production or M$_{1}$ receptor binding. AA inhibited both carbachol-induced transient and sustained increase in intracellular calcium concentration ([Ca$^{2+}$]$_{i}$; IC$_{50}$ = 11 and 12 μM, respectively). Furthermore, AA-induced increase in [Ca$^{2+}$]$_{i}$ cross-desensitizes with thapsigargin, but AA does not inhibit Ca$^{2+}$-ATPase activity. These data support the concept that AA concentration-dependently inhibits receptor-mediated NO production at the level of calcium mobilization.
Starting Page	441
Ending Page	449
Page Count	9
File Format	PDF
ISSN	03643190
Journal	Neurochemical Research
Volume Number	27
Issue Number	6
e-ISSN	15736903
Language	English
Publisher	Kluwer Academic Publishers-Plenum Publishers
Publisher Date	2002-01-01
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Neurosciences Neurology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Medicine Biochemistry Cellular and Molecular Neuroscience

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