HS-releasing compounds can increase outflow facility in porcine ocular anterior segment. The stimulatory action of these compounds on outflow is mediated, in part by endogenously produced HS, K channels, and adenylyl cyclase.

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Previous studies from our laboratory demonstrate that the hydrogen sulfide (H2S) donor, sodium hydrosulfide (NaHS) can increase aqueous humor (AH) outflow facility in porcine trabecular meshwork tissues, ex vivo. In the present study, we investigated the mechanism/s that underlie the NaHS‐induced increase in AH outflow facilityMethodsPorcine ocular anterior segments explants were perfused with Dulbecco's Modified Eagle's Medium maintained at 37° C, 5% CO2 and constant pressure of 7.35 mmHg. Once outflow was stable (~3 hours), explants were exposed to the adenylyl cyclase inhibitor SQ22536 (100 µM), enzyme inhibitors for H2S biosynthesis [proparglyglycine (PAG, 1 mM); aminooxyacetic acid (AOA, 30 µM)], and prostanoids (flurbiprofen, 3 µM), 30 minutes prior to application of NaHS (10 µM). Outflow was then monitored for an additional 4 hours, and vehicle control (0.1% saline) was run in parallel.ResultsThe NaHS‐induced increase in AH outflow was attenuated by AOA and PAG by 79% and 56%, respectively. In the presence of flurbiprofen (3 µM), effects of NaHS on outflow was significantly (p<0.02) inhibited from [130.6 ± 10.51% of basal] to [102.9 ± 2.88% of basal]. Furthermore, the adenylyl cyclase inhibitor, SQ22536 completely blocked (p <0.05) the NaHS‐induced increase in outflow facility.ConclusionWe conclude that the ability of NaHS to increase AH outflow in porcine trabecular meshwork is dependent upon the intramural generation of H2S and prostanoids, and on the integrity of the adenylyl cyclase pathway.