Abstract
A prior study found that inhibition of nitric oxide synthase with L-NAME causes a large, rapid decrease in IOP in anesthetized rabbits. In this follow-up study we sought to determine if this hypotensive effect was due to decreased aqueous production, possibly caused by ciliary vasoconstriction. Two protocols were performed in anesthetized rabbits. In the first protocol, mean arterial pressure (MAP) and IOP were measured by direct cannulation, and aqueous flow was measured by fluorophotometry, before and after L-NAME (5mgkg−1, i.v.,n=7). In the second protocol, ciliary blood flow was measured transclerally by laser Doppler flowmetry while MAP was varied mechanically over a wide range before and after L-NAME (5mgkg−1, i.v., n=8). L-NAME caused a significant increase in MAP and decreases in IOP, ciliary blood flow and aqueous flow. L-NAME also caused a significant downward shift in the ciliary pressure-flow relation over the entire pressure range examined. The results indicate that L-NAME causes ciliary vasoconstriction and decreases aqueous production, suggesting that the L-NAME ocular hypotensive effect may be due in part to a blood flow-dependent decrease in aqueous production. However, assuming no uveoscleral outflow and constant episcleral venous pressure and outflow facility, the decrease in aqueous flow accounts for 66% of the drop in IOP, suggesting an additional effect of L-NAME on aqueous outflow.