Phalloidin inhibits epinephrine's and cytochalasin B's facilitation of aqueous outflow
J. C. Robinson and P. L. Kaufman
Department of Ophthalmology and Visual Sciences, University of Wisconsin, Madison.
OBJECTIVE: To determine whether phalloidin, a fungal peptide that inhibits
actin filament depolymerization, could inhibit the ability of cytochalasin
B and epinephrine to increase the facility of aqueous outflow in the eyes
of living cynomolgus monkeys. METHODS: Outflow facility was determined by
two-level constant-pressure perfusion of the anterior chamber. After
measurement of baseline facility in both eyes, one eye of each animal
received intracameral phalloidin (1.3, 13, or 130 mumol/L); the opposite
eye received vehicle. Both eyes then received either epinephrine (0.3
mmol/L) or cytochalasin B (0.2 mmol/L), and facility was again measured.
RESULTS: Cytochalasin B and epinephrine increased facility by 120% to 190%
and 100% to 180%, respectively (uncorrected for 15% resistance washout
caused by perfusion itself). Phalloidin itself (13 or 130 mumol/L) did not
affect facility, but it inhibited up to 50% of the facility-increasing
effect of cytochalasin B and epinephrine. CONCLUSIONS: We conclude that (1)
the aqueous humor outflow facilitating effects of cytochalasin B or
epinephrine depend in some manner on depolymerization of actin filaments
within trabecular meshwork cells, and (2) actin filaments may help regulate
aqueous outflow.
