Nitric oxide enhances Ca2+-dependent K+ channel activity in rat carotid body cells

Jeane M. Silva, Deborah L. Lewis

Research output: Contribution to journalArticle

17 Scopus citations

Abstract

The nitric oxide (NO) donor S-nitroso-acetyl-penicillamine (SNAP) enhanced Ca2+-dependent K+ channel activity in rat carotid body chemoreceptor cells. Ca2+-dependent K+ channel activity was enhanced by SNAP in 38% (whole-cell configuration) and 67% (cell-attached mode) of the cells tested and was not affected by intracellular Ca2+ chelation with BAPTA-AM. Enhancement of Ca2+-dependent K+ channel activity by SNAP was blocked by the cGMP-dependent protein kinase G inhibitor 8-[(4-chlorophenyl)thio]-guanosine 3′,5′-cyclic monophosphothioate Rp diastereomer (Rp-8-pCPTcGMPS). NO thus enhances Ca2+-dependent K+ channel activity through cGMP-dependent protein kinase G. The NO-mediated increase in Ca2+-dependent K+ channel activity is likely to alter the function of carotid body chemoreceptor cells and could explain the decreased chemosensitivity of the carotid body in response to NO released from efferent nerves or vascular endothelial cells.

Original languageEnglish (US)
Pages (from-to)671-675
Number of pages5
JournalPflugers Archiv European Journal of Physiology
Volume443
Issue number5-6
DOIs
StatePublished - Mar 27 2002

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Keywords

  • BK channels
  • I
  • K+ channels
  • NO
  • Nitric oxide
  • SNAP

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Physiology (medical)

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