ABSTRACT
Calcium-activated, voltage-dependent Kþ channels, also called MaxiK or BKCa because of their large conductance (120 pS in physiological solutions), are abundant proteins in all smoothmuscles including the vasculature.MaxiK channels are key regulators of vascular tone, acting as a rheostat that fine-tunes the membrane potential and intracellular Ca2þ concentration according to the cell needs. Accordingly, MaxiK channels are targets of vasoactive substances including vasorelaxants (e.g., nitric oxide and arachidonic acid pathways) and vasoconstrictors (e.g., angiotensin II, 5-hydroxytryptamine, phenylephrine, thromboxane A2). A newly discovered pathway for vasoconstriction links constricting agonist stimulation to c-Src tyrosine kinase activation followed by phosphorylation and inhibition ofMaxiK channel activity, whichwould result in membrane depolarization, Ca2þ entry, and contraction. At the molecular level, MaxiK channels from vascular smooth muscle are formed by the coas-
Current affiliation: Department of Pharmacology, Yamagata University School of Medicine, Yamagata, Japan.
