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- W2000277552 abstract "The objective of the present study was to investigate if MAPK can be activated by a non-receptor agonist KCl, which depolarizes membrane to increase intracellular Ca(2+) and contracts cerebral arteries. Rabbit basilar arteries were used in isometric tension and western blot analysis studies. KCl produced a concentration-dependent contraction and an elevation of phospho-MAPK, which can be abolished by nicardipine, a voltage-dependent Ca(2+) channel blocker, and by PD98059 or U0126, MAPK kinase inhibitors. Thus, MAPK can be activated by the elevation of intracellular Ca(2+), independent of the activation of either G-protein coupled receptors or receptor tyrosine kinase. KCl which not only depolarizes membrane potentials, opens voltage-dependent Ca(2+), and increases intracellular Ca(2+), but also, probably by elevation of intracellular Ca(2+), triggers the activation of MAPK which seems responsible for a predominant part of the contraction of KCl in the rabbit basilar arteries." @default.
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- W2000277552 date "2002-04-01" @default.
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- W2000277552 title "KCl activates mitogen-activated protein kinase in rabbit bailar artery" @default.
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- W2000277552 doi "https://doi.org/10.1016/s0006-291x(02)00241-3" @default.
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