The effect of epinephrine on intraocular pressure (IOP) and the hemodynamics of the ciliary process vasculature in albino rabbits was studied by intraocular microendoscopy. Intraarterial application of epinephrine (15, 50, 250 ng/kg bw) lead to an immediate vasoconstriction and a reduction in blood flow velocity (BFV) in the iridial and major ciliary processes lasting from 30 to 120 sec. This anemic phase was followed by a hyperemic phase of about 60 to 240 sec. showing a vasodilation up to 150% of the initial diameters and an increase in BFV. The hyperemic phase can be prevented by pretreatment with indomethacin. Simultaneously measured IOP decreases in the anemic and increases in the hyperemic phase parallel with the changes in vascular diameter. After topical administration of epinephrine (25-50 micrograms/kg bw) a marked vasoconstriction followed by a vasodilatory phase was similarly found. However, the reactive changes of the ciliary process vasculature lasted considerably longer. The anemic phase lasted 15 minutes, the hyperemic phase 40 to 60 min. Again, this hyperemia can be prevented by indomethacin-pretreatment. In the iridial processes the anemic phase persisted till 70 minutes. No hyperemia and no substantial influence of indomethacin-pretreatment was found in this territory. In the anemic phase the IOP decreased in average from 20 mmHg to 15 mmHg. However, in contrast to the reactive changes of the IOP after intraarterial epinephrine application, the IOP did not increase again in the hyperemic phase, but decreased further to about 12 mmHg. After pretreatment with indomethacin the IOP remained at the level of 15 mmHg. The short-term IOP-changes after i.a. application of epinephrine, mirror the vasoconstrictory and vasodilatory reactions in the ciliary processes and might be due to volume changes in the eye (plethysmographic effect). However, the long lasting IOP reduction after topical epinephrine in the hyperemic phase can not be due to vascular reactions in the ciliary processes. There must be other factors responsible for the long lasting pressure reducing effect of epinephrine.