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Contribution of intra‐ and extracellular Ca 2+ to noradrenaline exocytosis induced by ouabain and monensin from guinea‐pig vas deferens
Author(s) -
Katsuragi Takeshi,
Ogawa Shusuke,
Furukawa Tatsuo
Publication year - 1994
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.1476-5381.1994.tb17063.x
Subject(s) - ouabain , monensin , cromakalim , chemistry , trifluoperazine , vas deferens , medicine , extracellular , endocrinology , intracellular , reserpine , nifedipine , channel blocker , calcium , biophysics , glibenclamide , biochemistry , biology , calmodulin , sodium , organic chemistry , diabetes mellitus
1 Contributions of intra‐ and extracellular Ca 2+ to noradrenaline (NA) release evoked by increasing intracellular Na + concentrations (ouabain plus monensin) from adrenergic nerves of guinea‐pig vas deferens were evaluated under conditions eliminating carrier‐mediated NA release (with 100 μ m cocaine). 2 Ouabain (100 μ m ) plus monensin (10 μ m ), unlike 100 m m KCl, produced a marked NA release which was unchanged by Ca 2+ ‐removal. 3 In normal solution but not in Ca 2+ ‐free solution, the release of NA evoked by ouabain plus monensin was reduced by adenosine, clonidine and neuropeptide Y, and by Ca 2+ ‐channel blockers such as ω‐conotoxin GVIA and nifedipine. The release of NA was also decreased by cromakalim in a glibenclamide‐sensitive fashion. 4 In contrast, in the absence but not in the presence of Ca 2+ , the drug‐evoked NA release was inhibited by mitochondrial inhibitors (carbonylcyanide‐ m ‐chlorophenylhydrazone and olivomycin) and further by immobilizers of intracellular Ca 2+ (TMB‐8 and BAPTA‐AM) and calmodulin antagonists (W‐7 and trifluoperazine). 5 These findings suggest that the release of NA evoked by elevation of [Na + 1 from adrenergic nerves in the presence and absence of Ca 2+ involves, in part, exocytotic processes which are triggered by depolarization‐induced Ca 2+ influx and by utilization of Ca 2+ from intracellular Ca 2+ store sites such as mitochondria, respectively.