title: KCl activates mitogen-activated protein kinase in rabbit bailar artery.
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.
authors.affiliation: Department of Neurosurgery, University of Mississippi Medical Center, Jackson, MS 39216, USA.
authors.forename: Alexander Y
authors.initials: AY
authors.lastname: Zubkov
authors.forename: K Shadon
authors.initials: KS
authors.lastname: Rollins
authors.forename: John H
authors.initials: JH
authors.lastname: Zhang
mesh_terms: D000818:Animals; D001488:Basilar Artery / Q000201:enzymology*; D004789:Enzyme Activation; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005260:Female; D005419:Flavonoids / Q000494:pharmacology; D007700:Kinetics; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000378:metabolism*; D009529:Nicardipine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology*; D011817:Rabbits
chemical_list: D004791:Enzyme Inhibitors; D005419:Flavonoids; D011189:Potassium Chloride; D009529:Nicardipine; D020928:Mitogen-Activated Protein Kinases; C093973:2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one