Membrane depolarization activates BK channels through ROCK-mediated β1 subunit surface trafficking to limit vasoconstriction

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Science Signaling  09 May 2017:
Vol. 10, Issue 478, eaah5417
DOI: 10.1126/scisignal.aah5417

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Trafficking patterns for vasodilation

Constriction of the small arteries that regulate regional organ blood flow occurs due to membrane depolarization of arterial myocytes, which stimulates voltage-dependent Ca2+ channels that mediate the influx of Ca2+ ions. Dilation of these blood vessels from the constricted state can occur due to BK channels, which are activated by Ca2+, partially reversing the membrane depolarization of arterial myocytes. Leo et al. found that membrane depolarization triggered a signaling pathway that ensured the activation of BK channels. Ca2+ influx through voltage-dependent Ca2+ channels activated kinases that increased the trafficking of the β1 auxiliary subunit of the BK channel to the plasma membrane, where it bound to the pore-forming subunit to increase its sensitivity to Ca2+. Thus, BK channels are activated in depolarized arterial myocytes not only because of direct stimulation by Ca2+, but also because of the increased plasma membrane abundance of the subunit that determines their sensitivity to Ca2+.

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