ADRENERGIC REGULATION OF AQUEOUS OUTFLOW

Epinephrine increased outflow facility and cyclic AMP in the in vitro perfused human anterior segment with a maximal facility increase of 44 % occurring at approximately 2 x 10(-5) M. Cyclic AMP measured in the perfusate from anterior segments increased by 12 - 14 fold after admin istration of 10(-5) M epinephrine. Both the facility increase and cycl ic AMP rise were blocked by the beta-2 selective antagonist, ICI118,55 1. While there was a correlation between the facility increase and ele vation in cyclic AMP levels, the rise in cyclic AMP preceded the facil ity increase by about 1 hour, suggesting that the ultimate effect of e pinephrine involved a rather slow event such as synthesis and release of prostaglandins or protein synthesis. Subsequent perfusion studies s howed that very large concentrations of indomethacin were necessary to block the outflow facility effect of epinephrine, suggesting that pro staglandin synthesis did not underlie the facility effect in this syst em. However, 5 x 10(-5) M cyclohexamide blocked the effect on outflow facility of both epinephrine and forskolin, but did not block the rise in cyclic AMP. These studies suggest that protein synthesis may play a role in the epinephrine-induced facility increase at some point beyo nd the second messenger level.