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Discrete store‐operated calcium influx into an intracellular compartment in rabbit arteriolar smooth muscle
Author(s) -
Flemming R.,
Cheong A.,
Dedman A. M.,
Beech D. J.
Publication year - 2002
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2002.023366
Subject(s) - serca , extracellular , chemistry , intracellular , fura 2 , endoplasmic reticulum , vasodilation , calcium , vascular smooth muscle , population , medicine , biophysics , endocrinology , cytosol , atpase , biology , biochemistry , smooth muscle , enzyme , organic chemistry , environmental health
This study tested the hypothesis that store‐operated channels (SOCs) exist as a discrete population of Ca 2+ channels activated by depletion of intracellular Ca 2+ stores in cerebral arteriolar smooth muscle cells and explored their direct contractile function. Using the Ca 2+ indicator fura‐PE3 it was observed that depletion of sarcoplasmic reticulum (SR) Ca 2+ by inhibition of SR Ca 2+ ‐ATPase (SERCA) led to sustained elevation of [Ca 2+ ] i that depended on extracellular Ca 2+ and slightly enhanced Mn 2+ entry. Enhanced background Ca 2+ influx did not explain the raised [Ca 2+ ] i in response to SERCA inhibitors because it had marked gadolinium (Gd 3+ ) sensitivity, which background pathways did not. Effects were not secondary to changes in membrane potential. Thus SR Ca 2+ depletion activated SOCs. Strikingly, SOC‐mediated Ca 2+ influx did not evoke constriction of the arterioles, which were in a resting state. This was despite the fura‐PE3‐indicated [Ca 2+ ] i rise being greater than that evoked by 20 m m [K + ] o (which did cause constriction). Release of endothelial vasodilators did not explain the absence of SOC‐mediated constriction, nor did a change in Ca 2+ sensitivity of the contractile proteins. We suggest SOCs are a discrete subset of Ca 2+ channels allowing Ca 2+ influx into a ‘non‐contractile’ compartment in cerebral arteriolar smooth muscle cells.