Large conductance, Ca2+-activated K+ channels (BKCa) and arteriolar myogenic signaling.

Michael A Hill, Yan Yang, Srikanth R Ella, Michael J Davis, Andrew P Braun

Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA. hillmi@missouri.edu

FEBS letters 2010 May 17

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Myogenic, or pressure-induced, vasoconstriction is critical for local blood flow autoregulation. Underlying this vascular smooth muscle (VSM) response are events including membrane depolarization, Ca(2+) entry and mobilization, and activation of contractile proteins. Large conductance, Ca(2+)-activated K(+) channel (BK(Ca)) has been implicated in several of these steps including, (1) channel closure causing membrane depolarization, and (2) channel opening causing hyperpolarization to oppose excessive pressure-induced vasoconstriction. As multiple mechanisms regulate BK(Ca) activity (subunit composition, membrane potential (Em) and Ca(2+) levels, post-translational modification) tissue level diversity is predicted. Importantly, heterogeneity in BK(Ca) channel activity may contribute to tissue-specific differences in regulation of myogenic vasoconstriction, allowing local hemodynamics to be matched to metabolic requirements. Knowledge of such variability will be important to exploiting the BK(Ca) channel as a therapeutic target and understanding systemic effects of its pharmacological manipulation. Copyright 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

Citation

Michael A Hill, Yan Yang, Srikanth R Ella, Michael J Davis, Andrew P Braun. Large conductance, Ca2+-activated K+ channels (BKCa) and arteriolar myogenic signaling. FEBS letters. 2010 May 17;584(10):2033-42