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ATP release evoked by isoprenaline from adrenergic nerves of guinea pig atrium

Authors
Journal
Neuroscience Letters
0304-3940
Publisher
Elsevier
Publication Date
Volume
186
Identifiers
DOI: 10.1016/0304-3940(95)11290-d
Keywords
  • Neuronal Atp Release
  • Isoprenaline
  • Presynapticβ2-Adrenoceptors
  • Ca2+/Calmodulin Antagonists
  • Myosin Light Chain Kinase Inhibitors
  • Guinea Pig Atrium

Abstract

Abstract Mode and site of release of ATP evoked by isoprenaline were evaluated in the electrically driven left atrial segment of guinea pig. The peak release of ATP 5 min after 1 μM isoprenaline was inhibited by 1 μM propranolol and 1 μM butoxamine, but not by 1 μM atenolol, showing that the ATP release is due to simulation of the presynaptic β 2-adrenoceptor by isoprenaline. The maximum ATP release was markedly reduced by Ca 2+/calmodulin antagonists, W-7 and trifluoperazine, and by a mitotic inhibitor, vinblastine. Further, the release was similarly inhibited by myosin light chain kinase inhibitors, ML-7 and wortmannin. Nifedipine, a Ca 2+-channel blocker, decreased the release of ATP evoked by isoprenaline. By contrast, Bay K 8644, a Ca 2+-channel opener, tended to enhance the ATP release. These findings suggest that isoprenaline produces ATP release from adrenergic nerve terminals of atrium, implying that ATP serves as a co-transmitter.

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