Adrenoceptor mechanisms in epinephrine-induced anterior choroidal vasoconstriction in cats.

These studies were undertaken to determine the role of epinephrine in the anterior choroidal circulation and to define the relative contribution of adrenoceptor subtypes in this response. Intra-arterial administration of l-epinephrine (0.03-1 microgram) produced vasoconstrictor responses in the anterior choroid of anesthetized cats as measured using laser-Doppler flowmetry. Ipsilateral nictitating membrane contractions were simultaneously recorded. Responses of both organs were blocked by intravenous treatment with the non-selective alpha-adrenoceptor antagonist phentolamine; however, only nictitating membrane contractions were significantly antagonized with the selective alpha 1-adrenoceptor antagonist, prazosin. In contrast, alpha 2-adrenoceptor blockade with rauwolscine had no depressant effect on the nictitating membrane but was a potent antagonist for epinephrine-induced ocular vasoconstriction. This differential ocular receptor type activation was confirmed with the use of more selective alpha-adrenoceptor agonists. Both the alpha 1-adrenoceptor agonist, methoxamine, and the selective alpha 2-adrenoceptor stimulant, B-HT 933, produced choroidal vasoconstriction when given intra-arterially. B-HT 933 was as potent as methoxamine in producing choroidal vasoconstriction which suggests a high ratio of alpha 2-adrenoceptors in this vascular bed. B-HT 933 was much less potent than methoxamine in producing contraction of the nictitating membrane. These results demonstrate the usefulness of laser-Doppler flowmetry in studies of the choroidal circulation and suggest that, unlike the nictitating membrane, epinephrine-induced anterior segment vasoconstriction is mediated by both postjunctional alpha 1- and alpha 2-adrenoceptors with alpha 2-adrenoceptors being predominant.