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Large conductance, Ca-activated K channels (BKCa) and arteriolar myogenic signaling
Authors:Michael A Hill  Yan Yang  Michael J Davis  Andrew P Braun
Institution:a Dalton Cardiovascular Research Center, University of Missouri, Columbia, MO 65211, USA
b Department of Medical Pharmacology and Physiology, University of Missouri, Columbia, MO 65211, USA
c Department of Biological Engineering, University of Missouri, Columbia, MO 65211, USA
d Department of Physiology and Pharmacology, University of Calgary, Calgary, Canada AB T2N 4N1
Abstract:Myogenic, or pressure-induced, vasoconstriction is critical for local blood flow autoregulation. Underlying this vascular smooth muscle (VSM) response are events including membrane depolarization, Ca2+ entry and mobilization, and activation of contractile proteins. Large conductance, Ca2+-activated K+ channel (BKCa) 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 BKCa activity (subunit composition, membrane potential (Em) and Ca2+ levels, post-translational modification) tissue level diversity is predicted. Importantly, heterogeneity in BKCa 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 BKCa channel as a therapeutic target and understanding systemic effects of its pharmacological manipulation.
Keywords:BKCa  large conductance  Ca2+-activated K+ channel  CICR  Ca2+-induced Ca2+ release  EC  endothelial cell  Em  membrane potential  IBTX  iberiotoxin  IK  intermediate conductance  Ca2+-activated K+ channel  IP3  inositol triphosphate  MLC  myosin light chain  PIP2  phosphatidylinositol 4  5-bisphosphate  PLC  Phospholipase C  RCK  regulator of conductance for K+  ROS  reactive oxygen species  RyR  ryanodine receptor  SK  small conductance  Ca2+-activated K+ channel  SR  sarcoplasmic reticulum  STOC  spontaneous transient outward current  STREX  STRess axis regulated EXon  VGCC  voltage-gated Ca2+ channel  VSD  voltage sensor domain  VSM  vascular smooth muscle
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