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

FEBS Lett. 2010 May 17;584(10):2033-42. doi: 10.1016/j.febslet.2010.02.045. Epub 2010 Feb 20.

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, 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.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Arterioles / cytology*
  • Arterioles / metabolism*
  • Arterioles / physiology
  • Blood Pressure*
  • Electrophysiological Phenomena
  • Humans
  • Large-Conductance Calcium-Activated Potassium Channels / chemistry
  • Large-Conductance Calcium-Activated Potassium Channels / metabolism*
  • Signal Transduction*

Substances

  • Large-Conductance Calcium-Activated Potassium Channels