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Ionic currents and inhibitory effects of glibenclamide in seminal vesicle smooth muscle cells
Author(s) -
Sadraei H.,
Beech D.J.
Publication year - 1995
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1995.tb16636.x
Subject(s) - tetraethylammonium , depolarization , pipette , chemistry , egta , biophysics , glibenclamide , voltage clamp , current clamp , membrane potential , nifedipine , reversal potential , channel blocker , patch clamp , calcium , endocrinology , potassium , biochemistry , biology , organic chemistry , diabetes mellitus , receptor
1 Whole‐cell voltage‐clamp recordings were made from smooth muscle cells isolated from guinea‐pig seminal vesicle. 2 When the recording pipette solution contained 130 m M KC1 and a low concentration of EGTA (0.2 mM), a dominant outward current was elicited by depolarization to positive of −30 mV from a holding potential of −50 mV. The current was non‐inactivating, stimulated by intracellular Ca 2+ and blocked by bath‐applied 1 m M tetraethylammonium but not 1 m M 3, 4 diaminopyridine. 3 If 10 m M EGTA was added to the KC1 pipette solution and the holding potential was −50 mV, or more negative, the major current elicited by depolarization to positive of −30 mV was an A‐type Re current. This current inactivated rapidly (within 100 ms) and was blocked by bath‐applied 1 m M 3, 4‐diaminopyridine but not 10 m M tetraethylammonium. 4 An inward voltage‐gated Ca channel current was observed on depolarization to positive of − 30 mV with 1.5 m M Ca 2+ or 10 m M Ba 2+ in the bath solution and when Cs + replaced K + in the pipette. The Ba 2+ ‐current was shown to be abolished by bath‐applied 100 μ m Cd 2+ and inhibited by 90% by 1 μ m nifedipine, and thus appeared to be carried by L ‐type Ca channels. 5 High concentrations of glibenclamide (10–500 μ m ) inhibited A‐type K + ‐current, Ba 2+ ‐current and contraction of the whole tissue induced by noradrenaline or electrical field stimulation. 6 From these data we suggest that seminal vesicle smooth muscle cells express Ca 2+ ‐dependent K channels, A‐type K channels and L ‐type Ca channels which are inhibited by tetraethylammonium, 3, 4‐diaminopyridine and nifedipine, respectively. In addition, an unexpected relaxant effect of high concentrations of glibenclamide may be explained by inhibition of the Ca channels.