Abstract
PURPOSE. The alpha(1A) adrenoceptor (alpha(1A)-AR) subtype was suggested to mediate contraction and trophic effects in the iris dilator muscle, and thus its pharmacological blockade may be involved in intraoperative floppy iris syndrome. We tested the hypothesis that the a1A-AR mediates pupil dilation and trophic effects in the mouse iris. METHODS. The alpha(1)-AR subtype mRNA expression was ...
Abstract
PURPOSE. The alpha(1A) adrenoceptor (alpha(1A)-AR) subtype was suggested to mediate contraction and trophic effects in the iris dilator muscle, and thus its pharmacological blockade may be involved in intraoperative floppy iris syndrome. We tested the hypothesis that the a1A-AR mediates pupil dilation and trophic effects in the mouse iris. METHODS. The alpha(1)-AR subtype mRNA expression was quantified in iris tissue by real-time PCR. To assess the role of individual a1-ARs for mediating pupil dilation, the a1-AR agonist phenylephrine was topically applied to the ocular surface of mice deficient in one of the three alpha(1)-AR subtypes (alpha(1A)-AR(-/-), alpha(1B)-AR(-/-), alpha(1D)-AR(-/-), respectively) and wild-type controls. Changes in pupil diameter were measured under a microscope in restrained mice. Moreover, iris and iris muscle thickness were determined in cryosections. RESULTS. Messenger RNA for all three alpha 1-AR subtypes was detected the iris of wild-type mice with a rank order of abundance of alpha(1A) >= alpha(1B) > > alpha(1D). The lack of a single alpha(1)-AR gene did not affect mRNA expression of the remaining two receptor subtypes. Phenylephrine induced pupil dilation in wild-type mice that was reduced in extent and duration in alpha(1A)-AR(-/)-and, less so, in alpha(1B)-AR(-/)- but not in alpha(1D)-AR(-/)-mice. The lack of a single alpha(1)-AR subtype had no effect on iris or iris muscle thickness. CONCLUSIONS. The a1-AR-induced mydriasis in mice is mediated mainly by the alpha(1A)-AR, with a smaller contribution of the alpha(1B)-AR, matching the relative abundance of these subtypes at the mRNA level. The lack of a single alpha(1)-AR subtype does not appear to cause atrophy in the mouse iris.
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