Uncoupling of neurovascular communication after transient global cerebral ischemia is caused by impaired parenchymal smooth muscle Kir channel function

J Cereb Blood Flow Metab. 2016 Jul;36(7):1195-201. doi: 10.1177/0271678X16638350. Epub 2016 Apr 6.

Abstract

Transient global cerebral ischemia is often followed by delayed disturbances of cerebral blood flow, contributing to neuronal injury. The pathophysiological processes underlying such disturbances are incompletely understood. Here, using an established model of transient global cerebral ischemia, we identify dramatically impaired neurovascular coupling following ischemia. This impairment results from the loss of functional inward rectifier potassium (KIR) channels in the smooth muscle of parenchymal arterioles. Therapeutic strategies aimed at protecting or restoring cerebrovascular KIR channel function may therefore improve outcomes following ischemia.

Keywords: KIR channel; Neurovascular coupling; cerebral blood flow; ischemia; smooth muscle.

Publication types

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

MeSH terms

  • Animals
  • Arterioles / metabolism*
  • Arterioles / physiopathology
  • Cerebrovascular Circulation / physiology
  • Endothelium, Vascular
  • Ischemic Attack, Transient / metabolism
  • Ischemic Attack, Transient / physiopathology*
  • Male
  • Muscle, Smooth, Vascular / metabolism*
  • Muscle, Smooth, Vascular / physiopathology
  • Neurovascular Coupling / physiology*
  • Parenchymal Tissue / blood supply*
  • Potassium Channels, Inwardly Rectifying / metabolism*
  • Rats, Sprague-Dawley

Substances

  • Potassium Channels, Inwardly Rectifying