Prejunctional α₂-adrenoceptors and peroxide-induced potentiation of norepinephrine release from the bovine iris

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 α₂-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. α₂-Adrenoceptor agonists, oxymetazoline, UK-14304 and clonidine inhibited field-stimulated [³H]NE overflow without affecting basal tritium efflux. Pretreatment of tissues with H₂O₂ (300 μM) had no effect on inhibition of evoked [³H]NE release caused by the α₂-adrenergic agonists. However, H₂O₂ (300 μM) caused significant (P <0.01) leftward shifts of excitatory concentration-response curves to yohimbine (10 nM-1 μM). In contrast, yohimbine (1 μM) did not prevent the enhancement of evoked [³H]NE overflow induced by H₂O₂ (300 μM). In conclusion, excitatory effects of peroxides on sympathetic neurotransmission in bovine irides are not mediated by prejunctional α₂-adrenoceptors.