Open AccessAcidosis Dilates Brain Parenchymal Arterioles by Conversion of Calcium Waves to Sparks to Activate BK Channels
Author(s) -
Fabrice Dabertrand,
Mark T. Nelson,
Joseph E. Brayden
Publication year - 2011
Publication title -
circulation research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.899
H-Index - 336
eISSN - 1524-4571
pISSN - 0009-7330
DOI - 10.1161/circresaha.111.258145
Subject(s) - bk channel , ryanodine receptor , chemistry , vascular smooth muscle , vasodilation , cerebral circulation , acidosis , arteriole , calcium activated potassium channel , dilator , medicine , calcium , nitric oxide , microcirculation , potassium channel , cerebral arteries , biophysics , endocrinology , biology , smooth muscle , organic chemistry
Acidosis is a powerful vasodilator signal in the brain circulation. However, the mechanisms by which this response occurs are not well understood, particularly in the cerebral microcirculation. One important mechanism to dilate cerebral (pial) arteries is by activation of large-conductance, calcium-sensitive potassium (BK(Ca)) channels by local Ca(2+) signals (Ca(2+) sparks) through ryanodine receptors (RyRs). However, the role of this pathway in the brain microcirculation is not known.
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