Endothelium-derived nitric oxide protection of spontaneous coronary contractions in the rabbit by countering Ca2+ influx via the voltage-sensitive Ca2+ channel.
The mechanism of spontaneous coronary contractions was investigated in the rabbit. Arteries with intact endothelium did not spontaneously contract. However, spontaneous coronary contractions were generated after the removal of the endothelium. NG-nitro-L-arginine methyl ester and methylene blue, the inhibitors of the formation and the action of nitric oxide, respectively, induced contractions in endothelium-intact arteries. Spontaneously produced contractions in endothelium-denuded arteries were reversibly inhibited by a Ca(2+)-free solution and by nifedipine, but not by inhibitors of neurotransmitters or prostanoids. These findings may indicate that spontaneous coronary contractions in the rabbit may be attributed to Ca2+ influx via the voltage-sensitive Ca2+ channel. The basal release of endothelium-derived nitric oxide may, in part, antagonize this Ca2+ influx.
Omote
M
M
Marion Merrell Dow, Osaka, Japan.
Mizusawa
H
H
D000818:Animals; D002118:Calcium / Q000378:metabolism; D015220:Calcium Channels / Q000378:metabolism; D003331:Coronary Vessels / Q000187:drug effects*; D004730:Endothelium, Vascular / Q000502:physiology; D008297:Male; D008564:Membrane Potentials; D009569:Nitric Oxide / Q000494:pharmacology*; D011817:Rabbits; D014661:Vasoconstriction / Q000187:drug effects*
D015220:Calcium Channels; D009569:Nitric Oxide; D002118:Calcium