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Nitric oxide directly activates calcium-dependent potassium channels in vascular smooth muscle.

Authors
  • Bolotina, V M
  • Najibi, S
  • Palacino, J J
  • Pagano, P J
  • Cohen, R A
Type
Published Article
Journal
Nature
Publication Date
Apr 28, 1994
Volume
368
Issue
6474
Pages
850–853
Identifiers
PMID: 7512692
Source
Medline
License
Unknown

Abstract

Nitric oxide is the major endothelium-derived relaxing factor (EDRF), and it is thought to relax smooth muscle cells by stimulation of guanylate cyclase, accumulation of its product cyclic GMP, and cGMP-dependent modification of several intracellular processes, including activation of potassium channels through cGMP-dependent protein kinase. Here we present evidence that both exogenous nitric oxide and native EDRF can directly activate single Ca(2+)-dependent K+ channels (K+Ca) in cell-free membrane patches without requiring cGMP. Under conditions when guanylate cyclase was inhibited by methylene blue, considerable relaxation of rabbit aorta to nitric oxide persisted which was blocked by charybdotoxin, a specific inhibitor of K+Ca channels. These studies demonstrate a novel direct action of nitric oxide on K+Ca channels.

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