Previous studies have shown that transmural electrical stimulation (TES) of the rabbit portal vein in vitro, results in the overflow of 3H-purines from tissues prelabelled with 3H-adenosine. The purpose of the present study was to assess the possible sites which contribute to the TES-induced overflow of purines in this adrenergically innervated tissue. The contribution of postjunctional elements to purine overflow was assessed with the α1-adrenoceptor antagonist, prazosin. Prazosin (3 × 10–7 M) did not affect the release of 3H-norepinephrine but markedly reduced the TES-induced contraction. The release of 3H-purines was reduced by 20% by prazosin, indicating that approximately 80% of the release is independent of the α1-mediated postjunctional response and, therefore, probably originates from neuronal sites in the tissue. Two lines of evidence indicate that a considerable portion of the α1- adrenoceptor-independent release of 3H-purines (i.e., in the presence of prazosin) arises from adrenergic nerves. First, the fractional release of 3H-purines was enhanced and reduced, respectively, by the α2-adrenoceptor antagonist, yohimbine, and the α2-adrenoceptor agonist, clonidine, in concentrations (10–6 M) which did likewise to the fractional release of 3H-norepinephrine. Second, destruction of the adrenergic nerves by in vitro treatment with 6-hydroxydopamine reduced the fractional release of 3H-purines by 55 %. The release of purines which remains after 6-hydroxydopamine treatment may occur from non-adrenergic nerves.

Keywords:
Co-release, Purines, Norepinephrine, Prazosin, Yohimbine, Clonidine, 6-Hydroxydopamine
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© 1982 S. Karger AG, Basel
1982
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