Abstract
Ion channels in vascular smooth muscle cells control membrane potential, which is a major determinant of the intracellular Ca2+ concentration and thus vascular tone. Membrane potential is modulated by a complex collection of endogenous vasodilator and vasoconstrictor pathways that ultimately dictate regional vascular resistance, organ blood flow, and systemic arterial pressure. Membrane potential in vascular smooth muscle is dominated by multiple types of K+ channels including those regulated by Ca2+, voltage, and ATP.1 It is not surprising then that K+ channels in vascular smooth muscle have been studied extensively as targets in normal vasoregulatory pathways and as end-effectors gone awry in diseases. Most investigations to date have focused on traditional intracellular signaling systems (eg, cyclic nucleotides and their associated kinases2) and chronic changes in expression patterns (eg, downregulation of subunits3). Article, see p 650 In the present issue of Circulation Research , Zhai et al4 examine the novel hypothesis that endothelin-1 elicits vasoconstriction, in part, by rapidly altering the subunit composition of vascular smooth muscle K+ channels, thereby reducing their functional activity. The K+ channel under investigation is the large conductance Ca2+-activated K+ channel, known colloquially as BK (K+ channels of big conductance).1 The subunit composition of BK …
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