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Measurement of chloride flux associated with the myogenic response in rat cerebral arteries
Author(s) -
Doughty Joanne M.,
Langton Philip D.
Publication year - 2001
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 - 10.1111/j.1469-7793.2001.t01-1-00753.x
Subject(s) - efflux , nimodipine , contraction (grammar) , myogenic contraction , chemistry , cerebral arteries , depolarization , medicine , endocrinology , biophysics , biology , biochemistry , calcium , smooth muscle
1 Self‐referencing ion‐selective (SERIS) electrodes were used to measure the temperature and pressure dependence of Cl − efflux, during myogenic contraction of pressurized rat cerebral resistance arteries. 2 At room temperature (18–21 °C), a small, pressure‐independent Cl − efflux was measured. On warming to 37 °C, arteries developed pressure‐dependent myogenic tone, and this was associated with a pressure‐dependent increase in Cl − efflux ( n = 5 ). 3 Both myogenic tone and the pressure‐ and temperature‐dependent Cl − efflux were abolished on application of 10 μ m tamoxifen, a Cl − channel blocker (IC 50 3.75 ± 0.2 μ m ). Tamoxifen (10 μ m ) also prevented contraction to 60 m m K + , suggesting non‐specific effects of tamoxifen ( n = 5 ). 4 Myogenic tone was abolished by 2 μ m nimodipine, but Cl − efflux was unaffected. In the presence of nimodipine, 10 μ m tamoxifen still abolished pressure‐ and temperature‐dependant Cl − efflux ( n = 3 ). 5 In summary, a Cl − efflux can be measured from rat cerebral arteries, with a temperature dependence that is closely correlated with myogenic contraction. We conclude that Cl − efflux through Cl − channels contributes to the depolarization associated with myogenic contraction.