Summary
Vasa deferentia from mice were field-stimulated by trains of 10 pulses delivered at 0.5 Hz. The pulses elicited separate twitches, the first of which (corresponding to a single pulse) exceeded the following ones in height and width and often was clearly biphasic. α, β-Methylene-ATP 1 μmol/1 and suramin 100 μmol/1 caused almost identical changes. They reduced the height of the first twitch in the train by about one half and also reduced its width in a manner indicating that only the second, slow phase remained, but reduced much more markedly the following twitches in which now a small second, slow phase also became detectable. Idazoxan 0.1 μmol/1 or yohimbine 0.1 μmol/l, when added in the presence of a, β-methylene-ATP or suramin, further decreased the first twitch but enhanced twitches No. 2 to 10. These responses were then almost abolished by prazosin 0.1 μmol/l. Successive addition of prazosin 0.1 μmol/l and idazoxan 0.1 μmol/1 to previously untreated vasa deferentia depressed the response to the first pulse by about one half in a manner indicating that only the first, rapid phase remained, but had comparatively little effect on the responses to the subsequent pulses. Suramin 100 μmol/l almost abolished the contractions remaining in the presence of prazosin and idazoxan. The results indicate that the first, rapid phase of the neurogenic contractions elicited by single or low frequency pulses is mediated by ATP which substantially contributes to all responses in a train. The second, slow phase is mediated by noradrenaline which substantially contributes to the response to the first pulse only. The adrenergic contribution seems to be mediated by postjunctional α1- as well as a α2-adrenoceptors. Prejunctional α2-adrenergic autoinhibition depresses the release of both ATP and noradrenaline.
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von Kügelgen, I., Bültmann, R. & Starke, K. Effects of suramin and α,β-methylene ATP indicate noradrenaline-ATP co-transmission in the response of the mouse vas deferens to single and low frequency pulses. Naunyn-Schmiedeberg's Arch Pharmacol 340, 760–763 (1989). https://doi.org/10.1007/BF00169686
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DOI: https://doi.org/10.1007/BF00169686