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• W2016497871 abstract "Acute respiratory distress syndrome (ARDS) is associated with increased superoxide (O 2 •− ) formation in the pulmonary vasculature and negation of the bioavailability of nitric oxide (NO). Since NO inhibits NADPH oxidase expression through a cyclic GMP‐mediated mechanism, sildenafil, a type V phosphodiesterase inhibitor, may be therapeutically effective in ARDS through an augmentation of NO‐mediated inhibition of NADPH oxidase. Therefore, the effect of sildenafil citrate and NO‐donating sildenafil (NCX 911) on O 2 •− formation and gp91 phox (active catalytic subunit of NADPH oxidase) expression was investigated in cultured porcine pulmonary artery endothelial cells (PAECs). PAECs were incubated with 10 n M TXA 2 analogue, 9,11‐dideoxy‐9 α ,11 α ‐methanoepoxy‐prostaglandin F 2 α (U46619) (±sildenafil or NCX 911), for 16 h and O 2 •− formation measured spectrophometrically and gp91 phox using Western blotting. The role of the NO‐cGMP axis was studied using morpholinosydnonimine hydrochloride (SIN‐1), the diethylamine/NO complex (DETA‐NONOate), the guanylyl cyclase inhibitor, 1H‐{1,2,4}oxadiazolo{4,3‐ a }quinoxalin‐1‐one (ODQ), and the protein kinase G inhibitor, 8‐bromoguanosine‐3′,5′‐cyclic monophosphorothioate, Rp‐isomer (Rp‐8‐Br‐cGMPS). NO release was studied using a fluorescence assay and O 2 •− –NO interactions by measuring nitrites. After a 16‐h incubation with 10 n M U46619, both NCX 911 and sildenafil elicited a concentration‐dependent inhibition of O 2 •− formation and gp91 phox expression, NCX 911 being more potent (IC 50 ; 0.26 n M ) than sildenafil citrate (IC 50 ; 1.85 n M ). These inhibitory effects were reversed by 1 μ M ODQ and 10 μ M Rp‐8‐Br‐cGMPS. NCX 911 stimulated the formation of cGMP in PAECs and generated NO in a cell‐free system to a greater degree than sildenafil citrate. The inhibitory effect of sildenafil was augmented by 1 μ M SIN‐1 and blocked partially by the eNOS inhibitor 10 μ M N 5 ‐(1‐iminoethyl)‐ornithine (L‐NIO). Acutely, sildenafil and NCX 911 also inhibited O 2 •− formation, again blocked by 1 μ M ODQ. NCX 911 reacted with O 2 •− generated by xanthine oxidase, an effect that was inhibited by superoxide dismutase (500 U ml −1 ). Since O 2 •− formation plays contributory role in ARDS, both sildenafil citrate and NCX 911 may be indicated for treating ARDS through suppression of NADPH oxidase expression and therefore of O 2 •− formation and preservation of NO bioavailability. British Journal of Pharmacology (2005) 146 , 109–117. doi: 10.1038/sj.bjp.0706305" @default.
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• W2016497871 date "2005-09-01" @default.
• W2016497871 modified "2023-10-13" @default.
• W2016497871 title "Sildenafil citrate and sildenafil nitrate (NCX 911) are potent inhibitors of superoxide formation and gp91^phoxexpression in porcine pulmonary artery endothelial cells" @default.
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• W2016497871 doi "https://doi.org/10.1038/sj.bjp.0706305" @default.
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