These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Contribution of intra- and extracellular Ca2+ to noradrenaline exocytosis induced by ouabain and monensin from guinea-pig vas deferens.
    Author: Katsuragi T, Ogawa S, Furukawa T.
    Journal: Br J Pharmacol; 1994 Nov; 113(3):795-800. PubMed ID: 7858869.
    Abstract:
    1. Contributions of intra- and extracellular Ca2+ 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 microM cocaine). 2. Ouabain (100 microM) plus monensin (10 microM), unlike 100 mM 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 omega-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 Ca2+, the drug-evoked NA release was inhibited by mitochondrial inhibitors (carbonylcyanide-m-chlorophenylhydrazone and oligomycin) and further by immobilizers of intracellular Ca2+ (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+]i from adrenergic nerves in the presence and absence of Ca2+ involves, in part, exocytotic processes which are triggered by depolarization-induced Ca2+ influx and by utilization of Ca2+ from intracellular Ca2+ store sites such as mitochondria, respectively.
    [Abstract] [Full Text] [Related] [New Search]