Factors Influencing the Release of Purines and Norepinephrine in the Rabbit Portal Vein

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 to postjunctional elements to purine overflow was assessed with the alpha 1-adrenoceptor antagonist, prazosin. Prazosin (3 x 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 alpha 1-mediated postjunctional response and, therefore, probably originates from neuronal sites in the tissue. Two lines of evidence indicate that a considerable portion of the alpha 1-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 alpha 2-adrenoceptor antagonist, yohimbine, and the alpha 2-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.