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 language | English (US) |
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Pages (from-to) | 671-675 |
Number of pages | 5 |
Journal | Pflugers Archiv European Journal of Physiology |
Volume | 443 |
Issue number | 5-6 |
DOIs | |
State | Published - 2002 |
Keywords
- BK channels
- I
- K+ channels
- NO
- Nitric oxide
- SNAP
ASJC Scopus subject areas
- Physiology
- Clinical Biochemistry
- Physiology (medical)