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Intracellular Ca2+‐store depletion triggers a Na+ influx via SOCs in guinea pig tracheal smooth muscle
Author(s) -
RomeroMendez Ana Catalina,
AlgaraSuarez Paola,
SanchezArmass Sergio,
Mandeville Peter B,
Meza Ulises,
EspinosaTanguma Ricardo
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1206.1
Subject(s) - niflumic acid , chemistry , depolarization , thapsigargin , biophysics , nifedipine , channel blocker , intracellular , contraction (grammar) , egta , tetraethylammonium chloride , verapamil , calcium , biochemistry , endocrinology , potassium , biology , organic chemistry
Guinea pig epithelial‐free tracheal rings were incubated with an EGTA‐buffered Ca 2+ ‐free solution and the SR‐Ca 2+ ‐ATPase blocker thapsigargin (Tg) 1 uM in order to deplete the intracellular Ca 2+ stores and induce a contraction upon Ca 2+ readmission. The contraction was inhibited (in %) by (mean +/− se; n= 4): SKF‐96365 (100 uM) 66.3 +/− 4.4, TRIM (100 uμM) 41.3 +/− 5.2 (inhibitors of SOC); nifedipine (1 uM) 86.2 +/− 3.4, verapamil (10 uM) 76.9 +/− 5.9 (inhibitors of Ca V 1.2 channels) and niflumic acid (20 uM) 41.1 +/− 9.8 (inhibitor of the CaCC). Moreover, in Na + ‐free conditions (Na + substituted by NMDG) the contraction evoked by Ca 2+ readmission was significantly inhibited. The resulting contraction under these conditions was, in turn, importantly reduced by nifedipine and niflumic acid when Na + was replaced by NMDG + and eliminated by nifedipine but resistant to niflumic acid when Na + was replaced by Li + . These findings support the idea that SOCs are non‐selective cation channels that permit Na + entry leading to an increase in cytosolic [Na + ] and cell depolarization. Depolarization and the increase of intracellular Na + levels are key events that induce the Na + ‐Ca 2+ exchanger to switch to its reverse mode, promoting a Ca 2+ influx that, in turn, activates CaCC increasing the depolarization phenomena and therefore the opening Ca v 1.2 channels. Supported by CONACYT 62220 to RET, UM and SSA and UASLP C05‐FAI‐10‐3.24 to SSA.