The effects of a number of purinoceptor agonists and antagonists on the release of endogenous norepinephrine (NE) from electrically field-stimulated (2 ms, 4 Hz) rabbit ear arteries were determined. NE was quantified by high-performance liquid chromatography and electrochemical detection techniques. Both P1- and P2-purinoceptor agonists enhanced the release of NE in a concentration-dependent manner (0.1 microM-100 microM), the relative order of potency being beta, gamma-methylene ATP (beta gamma-mATP) > 2-chloroadenosine (2CA) > ATP > L-phenylisopropyl-adenosine > 2-methylthio ATP > 5'N-ethylcarboxamido-adenosine. Adenosine and alpha, beta-methylene ATP (alpha beta-mATP) at 100 microM did not significantly enhance the electrical field stimulation-evoked release of NE. None of drugs changed the spontaneous overflow of NE. Pretreatment with alpha beta-mATP (1, 10 microM), a P2x-purinoceptor desensitizing agent, and 8-sulfophenyl theophylline (8SPT; 1 and 10 microM), a P1-purinoceptor antagonist, caused a shift to right of the concentration-release curve for beta gamma-mATP. alpha beta-mATP and 8SPT did not by themselves significantly affect the spontaneous overflow and the electrical field stimulation-evoked release of NE. Pretreatment of alpha beta-mATP (30 microM) and 8SPT (30 microM) antagonized facilitation of NE release by 2CA (10 microM). The concentration-contraction curve for beta gamma-mATP (1-300 microM) in the rabbit ear artery was shifted to the right by alpha beta-mATP (30 microM) but not by 8SPT (30 microM).(ABSTRACT TRUNCATED AT 250 WORDS)