We then examined if/how genetic deletion of NOS3 in CAV1
−/− mice impacted aqueous humor outflow. The flow rate data were plotted as a function of IOP and compared with the data in DKO, WT, NOS3 KO, and CAV1 KO mice (
Fig. 4). In DKO mice, the outflow rate at 5, 12, 15, 19, and 27 mm Hg was 0.09 ± 0.01, 0.20 ± 0.01, 0.27 ± 0.04, 0.33 ± 0.03, and 0.44 ± 0.03 μL/min, respectively. In comparison, in CAV1 KO mice, the outflow rate was 0.05 ± 0.01, 0.13 ± 0.01, 0.16 ± 0.01, 0.19 ± 0.01, and 0.25 ± 0.01 μL/min, respectively. The conventional outflow facility (C
con), which is the slope of the flow rate versus pressure graph, was 0.0161 ± 0.0022 mm Hg (
n = 19), 0.0125 ± 0.0014 mm Hg (
n = 7), 0.0088 ± 0.0010 mm Hg (
n = 7), and 0.0084 ± 0.0008 μL/min/mm Hg (
n = 7) for the DKO, WT, NOS3 KO, and CAV1 KO mice, respectively. C
con of DKO mice was similar to WT controls (
P > 0.05). NOS3 deletion in CAV1
−/− mice resulted in a 1.9-fold increase in C
con in DKO mice compared with CAV1 KO mice.