[Nitric oxide activates Ca2+ activated potassium current in rat tail artery smooth muscle cells via cGMP-dependent mechanism].
Mechanisms of nitric oxide (NO) action on K(Ca) channels were investigated using patch-clamp technique and freshly isolated smooth muscle cells from rat tail artery. In whole-cell experiments, the outward current was increased 6,64-/+0,72-fold (n=10) by 100 microM sodium nitroprusside (SNP), which was significantly different compared with 1,07-/+0,03-fold (n=8) increase of the outward current by addition of experimental bath solution. In the presence of 300 nM iberiotoxin, the specific blocker of K(Ca) channels, the outward current was not altered by 100 microM SNP. In addition, in the presence of 1 microM Rp-8-Br-PET-CGWS, the specific protein kinase G-inhibitor, the outward current was not affected by 100 microM SNP. These results suggest that NO released from NO-donors stimulates K(Ca) current in rat tail artery smooth muscle cells by activating protein kinase G and not by direct effect on the channel 1.
Gribkova
I V
IV
Shubert
R
R
Serebriakov
V N
VN
D000200:Action Potentials; D000818:Animals; D001158:Arteries / Q000378:metabolism; D006152:Cyclic GMP / Q000378:metabolism*; D032389:Myocytes, Smooth Muscle / Q000378:metabolism*; D009569:Nitric Oxide / Q000378:metabolism*; D018408:Patch-Clamp Techniques; D024681:Potassium Channels, Calcium-Activated / Q000378:metabolism*; D051381:Rats; D011921:Rats, Inbred WKY
D024681:Potassium Channels, Calcium-Activated; D009569:Nitric Oxide; D006152:Cyclic GMP