Abstract The relationship between ciliary perfusion and aqueous production is poorly understood. It was recently reported that aqueous production decreases when ciliary blood flow is reduced by lowering the ocular perfusion pressure, and hypothesized that drug-induced reduction of ciliary blood flow would also decrease aqueous production. In the present study, we test this hypothesis with an α2 adrenergic agonist (brimonidine) formulated for topical application. When used acutely, brimonidine decreases intraocular pressure (IOP) by suppressing aqueous production, although its mechanism of action is unclear. The experiments were performed in four groups of anesthetized rabbits ( n=33) in which the following variables were measured: ocular mean arterial pressure (OMAP), IOP, orbital venous pressure (OVP), aqueous flow, ciliary blood flow, ciliary oxygen tension (PO 2), episcleral venous pressure (EVP), carotid blood flow and heart rate. The measurements were made before and after brimonidine (0.15%, 40 μl) was applied to the cornea. Brimonidine decreased IOP (−33%, p<0.01), aqueous flow (−39%, p<0.01), ciliary blood flow (−37%, p<0.01), EVP (−42%, p<0.01) and ciliary PO 2 (−32%, p<0.05). We conclude that topical brimonidine is a ciliary vasoconstrictor, and that α2 adrenergic agonist-induced decreases in ciliary blood flow decrease aqueous production.