Research into aqueous humour production and its control within the bovine eye

The isolated, perfused bovine eye model has a long proven track record as an established experimental model allowing the study of the physiology and pharmacology of aqueous humour. Wilson et al, 1993 have shown this model in numerous experiments to provide reproducible results, consistent with in vivo models. Shahidullah et aL (1995, 1999) have since taken the use of the model ftirther showing a number of categories of drugs that reduce aqueous production and hence intraocular pressure. Bradykinin (10-9 to 10-8M) suppressesaqueous humour formation (42-49% reduction). At higher concentrations (3x10-8Mand 10-7M) aqueous production appeared to be increased (8-15% increase).It is possible that suppression of aqueous humour formation persists at higher bradykinin concentrations but at higher concentrations leakage of fluid from the vascular compartment into the chamber of the eye occurs -breakdown of the blood- aqueous barrier. Bradykinin was found to act through the B2 receptor. WIN 64338 (3x10-8M), a B2 receptor antagonist, abolished the effect of bradykininon aqueous humour formation suppression (unpaired t-test: p0.1) suggesting that there is no tonic influence of endogenous nitric oxide in the bovine ciliary epithelium. Bradykinin appears to suppress aqueous humour formation via nitric oxide and cGMP since a soluble guanylate cyclase inhibitor (ODQ) also blocked the bradykinin- induced inhibition of aqueous humour formation (bradykinin (10-9M) alone 42% reduction, in presenceof ODQ (3x10-7M) 4% reduction: unpaired t-test p<0.004). The absence of ascorbate from the perfusate significantly reduced the inhibitory effect of bradykinin on aqueous humour production (bradykinin (10-9M) in presence ofascorbate 42% reduction, bradykinin (10-9M) in absence of ascorbate 5% reduction:unpaired t-test p