The aim of this study was to investigate the influence of substances t
hat increase intracellular cAMP levels on the aqueous humor outflow fa
cility (C) of isolated bovine anterior segments. Anterior segments wer
e perfused in vitro at a constant pressure of 10 mmHg for 270 min with
a general protocol as follows: 90 min control perfusion with DMEM, 90
min of experimental perfusion with DMEM containing the test drug(s),
and 90 min of postdrug-perfusion with DMEM, C was calculated as the ra
tio between the rate of medium inflow (mu l/min) and the perfusion pre
ssure (mmHg). Anterior segments can be perfused in vitro for up to 5 h
r without significantly modifying their C, The addition of epinephrine
, forskolin, dibutyryl-cAMP or isobutylmethylxanthine to the control p
erfusion medium elicited a significant increase of C. If, during isobu
tylmethylxanthine perfusion, forskolin or epinephrine was added, C inc
reased significantly. Finally, perfusion with indomethacin prior to ad
dition of epinephrine prevented the increase of C induced by epinephri
ne. Epinephrine, the adenylate cyclase activator forskolin, the cAMP a
nalog dibutyryl-cAMP, and the. phosphodiesterase inhibitor isobutylmet
hylxanthine all increase aqueous facility. It seems reasonable to susp
ect that the cAMP system is involved in epinephrine's effects on bovin
e trabecular meshwork cells. Moreover, the complete inhibition by indo
methacin of the outflow facility increase induced by epinephrine sugge
sts that prostaglandins may be involved in the outflow facility mechan
isms related to adrenoreceptor stimulation of trabecular meshwork cell
s. Copyright (C) 1996 Elsevier Science Ltd.