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ATP release evoked by isoprenaline from adrenergic nerves of guinea pig atrium
T Tokunaga1, T Katsuragi, C Sato
1Department of Pharmacology, School of Medicine, Fukuoka University, Japan.
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 microM isoprenaline was inhibited by 1 microM propranolol and 1 microM butoxamine, but not by 1 microM atenolol, showing that the ATP release is due to stimulation of the presynaptic beta 2-adrenoceptor by isoprenaline. The maximum ATP release was markedly reduced by Ca2+/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.