A STUDY FOR INTRACELLULAR CALCIUM REGULATING MECHANISMS IN ARTERIAL SMOOTH MUSCLE AND THE EFFECT OF ANESTHETICS ON THESE MECHANISMS

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The purpose of this study was to clarify the role of K^+ channels in vasodilator as well as constrictor responses, which regulate intracellular levels of Ca^<2+>, and to determine whether anesthetics may modify these vascular responses via K^+ channels in parenchymal cerebral arterioles.The studies on cerebral parenchymal arterioles in the rat brain slice were introduced. Halothane dilated cerebral arterioles contracted with prostaglandine F_<2α>. An ATP-sensitive K^+ channel opener, levcromakalim and calcitonin-gene related peptide dilated these arterioles, whereas an ATP-sensitive K^+ channel inhibitor glibenclamide abolished these vasodilator responses. A local anesthetic lidocaine inhibited vasodilation induced by levcromakalim, whereas it did not alter contraction in response to prostaglandine F_<2α>. Lidocaine did not affect vasodilation induced by a nitric oxide donor sodium nitroprusside.It appears that lidocaine may be selectively capable of inhibiting vasodilaiton mediated by ATP-sensitive K^+ channel s in cerebral parenchymal arterioles. These results suggest that anesthetics may modify the mechanisms to maintain cerebral blood flow by inducing vasodilation mediated by opening of ATP-sensitive K^+ channels, resulting in lowered intracellular levels of Ca^<2+>.