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.