Nitric oxide enhances Ca(2+)-dependent K(+) channel activity in rat carotid body cells.

The nitric oxide (NO) donor S-nitroso-acetylpenicillamine (SNAP) enhanced Ca(2+)-dependent K(+) channel activity in rat carotid body chemoreceptor cells. Ca(2+)-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 Ca(2+) chelation with BAPTA-AM. Enhancement of Ca(2+)-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-pCPT-cGMPS). NO thus enhances Ca(2+)-dependent K(+) channel activity through cGMP-dependent protein kinase G. The NO-mediated increase in Ca(2+)-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.