NEURAL ATP RELEASE AND ITS ALPHA-2-ADRENOCEPTOR-MEDIATED MODULATION IN GUINEA-PIG VAS-DEFERENS

Contractions, release of previously stored [H-3]-noradrenaline (measur ed as overflow of total tritiated compounds) and release of ATP elicit ed by electrical field stimulation (210 pulses, 7 Hz) were studied in the superfused vas deferens of the guinea pig. Prazosin and suramin we re used to suppress non-neural ATP release, and effects of bromoxidine and rauwolscine on the neural release thus isolated were examined. El ectrical stimulation elicited reproducible contraction, tritium overfl ow and ATP overflow. Both prazosin (0.03 - 3 muM) and suramin (30 - 30 0 muM) reduced contractions as well as the evoked overflow of ATP. No visible contraction remained in 21 of 28 tissues exposed to prazosin 0 .3 muM combined with suramin 300 muM. The evoked overflow of ATP under these conditions was about 17% of that observed in the absence of dru gs. In the presence of prazosin 0.3 muM and suramin 300 muM, bromoxidi ne (0.01 - 1 muM) decreased and rauwolscine (0.1 - 10 muM) increased t he evoked overflow of both tritium and ATP. Rauwolscine increased the evoked overflow of tritium to a significantly greater extent than the overflow of ATP. It is concluded that the overflow of ATP elicited by electrical (neural) stimulation in the presence of prazosin 0.3 muM an d suramin 300 muM reflects purely neural release of ATP. This release of ATP, like the release of noradrenaline, is modulated through prejun ctional alpha2-adrenoceptors. The alpha2-adrenoceptor modulation of th e release of noradrenaline seems to be more marked than the modulation of the release of ATP.