Interaction between the L-type Ca2+ channel and the Ca(2+)-activated K+ channel in the fluctuating myogenic contraction in the rabbit basilar artery.
Ring preparations of the rabbit basilar artery spontaneously developed a fluctuating contraction that was not inhibited by the removal of the endothelium or by blockade of the synthesis or action of neurotransmitters and prostanoids. Nifedipine greatly relaxed the spontaneously-developed contraction. Charybdotoxin, an antagonist of the Ca(2+)-activated K+ channel, converted the fluctuating contraction to a tonic contraction, whereas the ATP-sensitive K+ channel blocker, glibenclamide, had no effect. These results indicate that the increased Ca2+ influx via the L-type Ca2+ channel in the rabbit basilar artery may induce myogenic contraction and consequently activate the Ca(2+)-activated K+ channel, which might lead to the fluctuation of the contraction by feedback regulation of the Ca2+ channel.
Omote
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Marion Merrell Dow, Hirakata, Japan.
Mizusawa
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H
D000818:Animals; D001488:Basilar Artery / Q000187:drug effects / Q000502:physiology*; D002118:Calcium / Q000502:physiology*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000502:physiology*; D018999:Charybdotoxin / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000502:physiology*; D009543:Nifedipine / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000502:physiology*; D011817:Rabbits; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D018999:Charybdotoxin; D009543:Nifedipine; D005905:Glyburide; D002118:Calcium