Peroxides can enhance field-stimulated [3H]norepinephrine ([3H]NE) release in isolated irides from several mammalian species. In the present study, we investigated the role of prejunctional alpha2-adrenoceptors in peroxide-induced potentiation of sympathetic neurotransmission in bovine isolated irides. Isolated hemi-irides were incubated in a Krebs buffered-solution containing [3H]NE and prepared for studies of neurotransmitter release using the superfusion method. Alpha2-adrenoceptor agonists, oxymetazoline, UK-14304 and clonidine inhibited field-stimulated [3H]NE overflow without affecting basal tritium efflux. Pretreatment of tissues with H2O2 (300 microM) had no effect on inhibition of evoked [3H]NE release caused by the alpha2-adrenergic agonists. However, H2O2 (300 microM) caused significant (P < 0.01) leftward shifts of excitatory concentration-response curves to yohimbine (10 nM-1 microM). In contrast, yohimbine (1 microM) did not prevent the enhancement of evoked [3H]NE overflow induced by H2O2 (300 microM). In conclusion, excitatory effects of peroxides on sympathetic neurotransmission in bovine irides are not mediated by prejunctional alpha2-adrenoceptors.
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