Arachidonic acid inhibition of muscarinic receptor-mediated nitric oxide production occurs at the level of calcium mobilization in Chinese hamster ovary cells

David R. Linden, Esam E. El-Fakahany

Research output: Contribution to journalArticlepeer-review

2 Scopus citations

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. T he effects of exogenous AA on signal transduction of M1 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 (IC50 = 191 μM) but did not alter inositol phosphate production or M1 receptor binding. AA inhibited both carbachol-induced transient and sustained increase in intracellular calcium concentration ([Ca2+]i; IC50 = 11 and 12 μM, respectively). Furthermore, AA-induced increase in [Ca2+]i cross-desensitizes with thapsigargin, but AA does not inhibit Ca2+-ATPase activity. These data support the concept that AA concentration-dependently inhibits receptor-mediated NO production at the level of calcium mobilization.

Original languageEnglish (US)
Pages (from-to)441-449
Number of pages9
JournalNeurochemical Research
Volume27
Issue number6
DOIs
StatePublished - Jun 2002

Keywords

  • Arachidonic acid
  • Calcium signaling
  • Cross-talk
  • Muscarinic receptor
  • Nitric oxide
  • Second messengers
  • Signal transduction

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

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