Abstract

Effects of phenylephrine (α 1-adrenergic agonist), prazosin (α 1-adrenergic antagonist), clonidine (α 2-adrenergic agonist), and yohimbine (α 2-adrenergic antagonist) on aqueous humor (AH) dynamics were studied with a cat eye model. Phenylephrine (130 μg/ml) inhibited AH outflow (67% at 90 min. period) more than AH formation (26% at the same period) indicating the intraocular pressure (IOP) might be raised by the administration of phenylephrine. Prazosin (0.1 μg/ml) produced effects opposite to those of phenylephrine (55% reduction of AH formation and 25% reduction of AH outflow at 3 hr. period) suggesting the α 1-adrenergic receptor is responsible for increases rather than decreases of IOP. Both clonidine (10 μg/ml) and yohimbine (0.1–1.0 μg/ml) inhibited AH formation (60% inhibition) more than AH outflow (no inhibition for clonidine and 40% inhibition for yohimbine) to lower IOP. The conventional theory of receptor antagonism does not seem to function at α 2-receptor sites.

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