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Abstract
Ocular tension of cats was measured after topical administration of the selective beta 1-adrenergic agonist CGP 7760B, the selective beta 1-adrenergic antagonist atenolol, the selective beta 2-adrenergic agonist salbutamol, the selective beta 2-adrenergic antagonist H 35/25, and the mixed beta 1- and beta 2-adrenergic antagonist timolol. Although atenolol did not alter intraocular pressure, CGP 7760B produced a modest decrease amounting to 3 to 4 mm Hg. Salbutamol, H 35/25, and timolol each produced a dose-dependent lowering of ocular tension, with maximal reductions amounting to 7, 5, and 5 mm Hg, respectively. Sympathetically denervated cat eyes showed supersensitivity to the pressure-lowering effect of salbutamol. In contrast, sympathectomy markedly reduced the effects of H 35/25 and timolol on ocular tension. Eyes rendered subsensitive to the pressure-lowering effects of cholinomimetics by chronic echothiophate treatment likewise showed diminished responsiveness to H 35/25 and timolol. Pretreatment with timolol (3 hr) completely abolished the pressure-lowering effect of salbutamol, and pretreatment with atenolol likewise completely antagonized the effect of CGP 7760B. These results suggest that beta-adrenergic receptors in the anterior segment of the cat eye are predominantly beta 2. Although beta-adrenergic antagonists apparently exert their effects on ocular tension by action at beta-adrenergic receptors, a cholinergic mechanism may be involved as well.