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. 2011 Dec;339(3):815–824. doi: 10.1124/jpet.111.184416

Fig. 4.

Fig. 4.

ERα and ERβ activation results in NO production in human BECs. A, in DAF-2-loaded human BECs 20 μM ATP (shown) and 1 μM ACh (not shown) both induced an increase in NO production (15 min). Treatment with the nonselective physiologically relevant E2 (10 nM) or the ERα- versus ERβ-selective agonists (THC and DPN, respectively; 10 nM each) caused an increase in fluorescence comparable with that of ATP (20 μM). In comparison, the GPCR30 agonist G1 had no effect on fluorescence. B, amplitude of agonist or estrogen induced DAF-2 response. Based on the DAF-2 calibration in Fig. 2, NO levels were in the range of 30 to 85 nM. Vehicle control as well as G1 showed minimal change in fluorescence. C, rate of NO production. Estrogen-induced NO production was only slightly slower than that by ATP. In B and C, values are means ± S.E. (n = five patients). * indicates significant difference from vehicle control (p < 0.05). N.D., not determinable (rate of change was negligible).