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Cellular Physiology of Retinal and Choroidal Arteriolar Smooth Muscle Cells
Author(s) -
SCHOLFIELD C. N.,
MCGEOWN J. G.,
CURTIS T. M.
Publication year - 2007
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1080/10739680601072115
Subject(s) - chemistry , retinal , microbiology and biotechnology , biophysics , intracellular , neuroscience , biology , biochemistry
Control of ocular blood flow occurs predominantly at the level of the retinal and choroidal arterioles. The present article provides an overview of the Ca 2 + handling mechanisms and plasmalemmal ion channels involved in the regulation of retinal and choroidal arteriolar smooth muscle tone. Increases in global intracellular free Ca 2 + ([Ca 2 + ] i ) involve multiple mechanisms, including agonist‐dependent release of Ca 2 + from intracellular stores through activation of the inositol trisphosphate (IP 3 ) pathway. Ca 2 + enters by voltage‐dependent L‐type Ca 2 + channels and novel dihydropyridine‐sensitive store‐operated nonselective cation channels. Ca 2 + extrusion is mediated by plasmalemmal Ca 2 + ‐ATPases and through Na + /Ca 2+ exchange. Local Ca 2 + transients (Ca 2 + sparks) play an important excitatory role, acting as the building blocks for more global Ca 2 + signals that can initiate vasoconstriction. K + and Cl − channels may also affect cell function by modulating membrane potential. The precise contribution of each of these mechanisms to the regulation of retinal and choroidal perfusion in vivo warrants future investigation.