ABSTRACTThe IOP and pupil response to α-adrenergic agonists and blockers was studied in albino rabbits. Topical ocular application of solutions of methoxamine (α1) and oxymetazoline (α2) caused dose-related early rises in IOP which were inhibited by pretreatment with prazosin, an α1-blocker, or with yohimbine, an α2-blocker. Although both prazosin and yohimbine have ocular hypotensive activity, the effect on the early IOP rise did not appear to be related to this action. Prazosin and yohimbine also inhibited the early IOP rise after treatment with clonidine, a second α2-agonist. Surgically sympathectomized rabbits showed little or no hypersensitivity to methoxamine or oxymetazoline when compared to non-operated normal rabbits. However the treated ipsilateral eyes showed a much greater increase in IOP than the treated contralateral eyes. There was little difference in the IOP response between clonidine-treated ipsilateral and contralateral eyes. Methoxamine and oxymetazoline caused dose-related increases in the pupil diameter which were blocked by the nonselective α-blocker phentolamine but not by prazosin (α1) or yohimbine (α2). This study suggests: 1) That the early IOP rise after treatment with α-agonists is due to stimulation of postsynaptic α1-receptors, possibly located in superficial blood vessels in the anterior segment of the eye; 2) The mydriatic response to α-agonists appears to be mediated by α-receptors which differ from the classical α1a
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