Premium
Large conductance, Ca 2+ ‐activated K + channels (BK Ca ) and arteriolar myogenic signaling
Author(s) -
Hill Michael A.,
Yang Yan,
Ella Srikanth R.,
Davis Michael J.,
Braun Andrew P.
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.02.045
Subject(s) - bk channel , depolarization , vasoconstriction , hyperpolarization (physics) , biophysics , chemistry , myogenic contraction , vascular smooth muscle , autoregulation , membrane potential , biology , endocrinology , smooth muscle , blood pressure , stereochemistry , nuclear magnetic resonance spectroscopy
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.