ATP Release and its Prejunctional Modulation

  1. Derek J. Chadwick Organizer and
  2. Jamie A. Goode
  1. Klaus Starke,
  2. Ivar von Kügelgen,
  3. Bernd Driessen and
  4. Ralph Bültmann

Published Online: 28 SEP 2007

DOI: 10.1002/9780470514900.ch14

Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms

Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms

How to Cite

Starke, K., von Kügelgen, I., Driessen, B. and Bültmann, R. (2007) ATP Release and its Prejunctional Modulation, in Ciba Foundation Symposium 198 - P2 Purinoceptors: Localization, Function and Transduction Mechanisms (eds D. J. Chadwick and J. A. Goode), John Wiley & Sons, Ltd., Chichester, UK. doi: 10.1002/9780470514900.ch14

Author Information

  1. Pharmakologisches Institut, Albert Ludwigs-Universität Freiburg, Hermann-Herder-Strasse 5, D-79104 Freiburg im Breisgau, Germany

Publication History

  1. Published Online: 28 SEP 2007

ISBN Information

Print ISBN: 9780471961253

Online ISBN: 9780470514900

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Keywords:

  • ATP release;
  • prejunctional modulation;
  • prejunctional α2-adrenoceptors;
  • luciferin-luciferase technique

Summary

We studied some properties of the release of noradrenaline and ATP in isolated sympathetically innervated tissues. Release was elicited by electric stimulation and assessed as overflow of tritiated compounds (after labelling with [3H]noradrenaline) and enzymically measured ATP, respectively. Evans blue, which inhibits ectonucleotidases, greatly increased the evoked overflow of ATP, indicating that a major part of the ATP was metabolized after release. Much of the ATP was postjunctional in origin. The neural fraction was isolated when postjunctional release was suppressed by prazosin (α1-adrenoceptor antagonist) and suramin (P2 purinoceptor antagonist). Comparison of neural ATP and [3H]-noradrenaline release showed that prostaglandin E2 reduced the release of both co-transmitters to a similar extent. Activation of prejunctional α2-adrenoceptors, however, preferentially reduced the release of [3H]noradrenaline, and activation of prejunctional A1 purinoceptors reduced preferentially the release of ATP. Nucleotides such as ATP depressed the release of [3H]noradrenaline through two receptors: the well-known prejunctional A1 receptors and a separate group of prejunctional P2 purinoceptors. P2 antagonists increased the release of [3H]-noradrenaline. Overall, the results indicate differential storage, release and modulation of release of the two sympathetic co-transmitters. They also indicate that postganglionic sympathetic axons possess receptors for both co-transmitters: α2 and P2 autoreceptors.