Large conductance, Ca2+-activated K+ channels (BKCa) and arteriolar myogenic signaling.
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.
Hill
Michael A
MA
Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA. hillmi@missouri.edu
Yang
Yan
Y
Ella
Srikanth R
SR
Davis
Michael J
MJ
Braun
Andrew P
AP
D000818:Animals; D001160:Arterioles / Q000166:cytology* / Q000378:metabolism* / Q000502:physiology; D001794:Blood Pressure; D055724:Electrophysiological Phenomena; D006801:Humans; D051036:Large-Conductance Calcium-Activated Potassium Channels / Q000737:chemistry / Q000378:metabolism*; D015398:Signal Transduction
D051036:Large-Conductance Calcium-Activated Potassium Channels