Effect of volatile anesthetics on the ion-channels of the cerebral vascular smooth muscle isolated from dog

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(1) The rings of the dog cerebral artery without endothelium but not the mesenteric artery maintained an automatic myogenic tone in the resting state. The myogenic tone was abolished in the Ca^<++> free Ringer solution and in the presence of nifedipine. These findings suggest that the increased basal Ca^<++> influx through voltage-dependent Ca^<++> channel is responsible for the maintenance of myogenic tone in the cerebral artery. Halothane significantly inhibited the myogenic tone observed in the cerebral arterial rings.(2) The addition of tetraethylammonium and charybdotoxin (Ca^<++>-activated K^+ channel inhibitors) produced a concentration-dependent contraction in the cerebral artery, but not in the mesenteric artery. These findings suggest that Ca^<++>-activated K^+ channel was highly activated by the increased Ca^<++> influx in the cerebral artery. Halothane, even at a low concentration of 0.5 MAC,strongly attenuated the tension development elicited by tetraethylammonium and charybdotoxin.(3) Exposure of the mesenteric arterial rings precontracted with phenylephrine to halothane (4 MAC) caused a rapid contraction, which reached a plateau within 5 to 10 min. After stabilization, termination of halothane produced a transient and profound relaxation. This relaxation was inhibited by ouabain, a Na^+-K^+ ATPase inhibitor, in a concentration-dependent manner. Substitution of Li^+ for Na^+ in Ringer solution also attenuated the relaxation. These results suggest that the relaxation elicited by termination of halothane exposure may be responsible to an alteration of Na^+-K^+ ATPaes activity in the mesenteric artery.The effect of volatile anesthetics on the alteration of intracellular ion concentration (Na^+, Ca^<++>) is now under way in our laboratory.