Phalloidin Inhibits Epinephrine's and Cytochalasin B's Facilitation of Aqueous Outflow

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Abstract
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 μmol/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 μmol/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.