KCl activates mitogen-activated protein kinase in rabbit bailar artery

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 Ca²⁺ 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 Ca²⁺ channel blocker and by PD98059 or U0126 MAPK kinase inhibitors. Thus MAPK can be activated by the elevation of intracellular Ca²⁺ independent of the activation of either G-protein coupled receptors or receptor tyrosine kinase. KCl which not only depolarizes membrane potentials opens voltage-dependent Ca²⁺ and increases intracellular Ca²⁺ but also probably by elevation of intracellular Ca²⁺ triggers the activation of MAPK which seems responsible for a predominant part of the contraction of KCl in the rabbit basilar arteries.