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1 vial tissues and incubated with the NO donor S-nitroso-N-acetylpenicillamine.
2 ented the relaxation induced by the NO donor S-nitroso-N-acetylpenicillamine.
3 be restored by the addition of the NO donor S-nitroso-N-acetylpenicillamine.
4 tonic conditions with the nitric oxide donor S-nitroso-N-acetylpenicillamine.
6 F) cultures was inhibited by the addition of S-nitroso-N-acetylpenicillamine, a nitric oxide (NO)-gen
8 ly enhances M1 macrophage polarization while S-nitroso-N-acetylpenicillamine, a NO donor, suppresses
10 -diolate (NOC-18), S-nitrosoglutathione, and S-nitroso-N-acetylpenicillamine also suppressed CYP2B pr
11 tic antibody Jo2, a nitric oxide (NO) donor (S-nitroso-N-acetylpenicillamine), an NO inhibitor (N(G)-
12 ffects with those of the nitric oxide donor, S-nitroso-N-acetylpenicillamine, an agent we showed prev
13 duced response, the vasodilation elicited by S-nitroso-N-acetylpenicillamine, an NO donor that activa
14 posure of slices to the nitric oxide donors, S-nitroso-N-acetylpenicillamine and S-nitroso-glutathion
16 Aorta treated with the nitric oxide donors, S-nitroso-N-acetylpenicillamine and sodium nitroprusside
18 oxidized by NO donors, sodium nitroprusside, S-nitroso-N-acetylpenicillamine, and S-nitrosoglutathion
19 ionophore ionomycin, the nitric oxide donor S-nitroso-N-acetylpenicillamine, and the protein kinase
21 enerated by the addition of 400 microM SNAP (S-nitroso-N-acetylpenicillamine) caused a 10-fold increa
22 m nitroprusside inhibited HIV-PR by 70%, and S-nitroso-N-acetylpenicillamine completely inhibited the
25 nterestingly, treatment of EC with NO donor, S-nitroso-N-acetylpenicillamine, did not activate SREBP,
28 xyimino]-5-nitro-6-methoxy-3-hexeneamide and S-nitroso-N-acetylpenicillamine greatly enhanced the for
29 HeLa and COS-7 cells, the nitric oxide donor S-nitroso-N-acetylpenicillamine increased the activity o
31 , and the NO donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine mimicked CYP2B1 protein
33 cells were exposed to an exogenous NO donor, S-nitroso-N-acetylpenicillamine or a substrate inhibitor
34 nt of N18 neuroblastoma cells with NO donors S-nitroso-N-acetylpenicillamine or sodium nitroprusside
35 nted that the addition of NO donor molecules S-nitroso-N-acetylpenicillamine or sodium nitroprusside
36 -A promoter, in which the nitric oxide donor S-nitroso-N-acetylpenicillamine reduces urea transporter
38 a-dependent sensitization whereas NO donors (S-nitroso-N-acetylpenicillamine) sensitized these cells
40 Exogenous and endogenous sources of NO, from S-nitroso-N-acetylpenicillamine (SNAP) and bradykinin or
41 t cGMP-elevating agents such as the NO donor S-nitroso-N-acetylpenicillamine (SNAP) and C-type natriu
42 e phosphorylated in response to the NO donor S-nitroso-N-acetylpenicillamine (SNAP) and the activatio
44 nor compounds sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) both inhibited th
45 t not higher (100-500 mum), concentration of S-nitroso-N-acetylpenicillamine (SNAP) can reverse the e
47 ultures of rat hepatocytes with the NO donor S-nitroso-N-acetylpenicillamine (SNAP) induced the expre
49 the NO donors sodium nitroprusside (SNP) and S-nitroso-N-acetylpenicillamine (SNAP) on cell cycle act
50 The effects of authentic NO and the NO donor S-nitroso-N-acetylpenicillamine (SNAP) on swelling-activ
51 roprusside (SNP), S-nitroglutathione (GSNO), S-nitroso-N-acetylpenicillamine (SNAP) or 3-morpholinosy
52 e of SMC in culture to the nitrovasodilators S-nitroso-N-acetylpenicillamine (SNAP) or sodium nitropr
54 ine (CSNO), S-nitrosoglutathione (GSNO), and S-nitroso-N-acetylpenicillamine (SNAP) reversibly oxidiz
55 The vasodilation elicited by the NO donor S-nitroso-N-acetylpenicillamine (SNAP) was inhibited by
56 l death and nitrite levels at 24 h caused by S-nitroso-N-acetylpenicillamine (SNAP), a direct nitric
57 es or cytosol isolated from hepatocytes with S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide d
58 monophosphate (8-Br-cGMP), a cGMP analog or S-nitroso-N-acetylpenicillamine (SNAP), a NO donor essen
59 nors were used: spermine NONOate (SP), (+/-)-S-nitroso-N-acetylpenicillamine (SNAP), and S-nitrosoglu
60 O) mice, inducible NOS KO mice, the NO donor S-nitroso-N-acetylpenicillamine (SNAP), and the NOS inhi
61 treatment with the nitric oxide (NO) donor, S-nitroso-N-acetylpenicillamine (SNAP), and the phosphod
63 donors, diethylenetriamine/NO (DETA/NO) and S-nitroso-N-acetylpenicillamine (SNAP), at doses previou
65 donors, S-nitroglutathione (GSNO) and (+/-)-S-nitroso-N-acetylpenicillamine (SNAP), directly inhibit
66 eurons (CGNs) by treatment with the NO donor S-nitroso-N-acetylpenicillamine (SNAP), for short (6 h)
67 chelatase incubated with NO or the NO donor, S-nitroso-N-acetylpenicillamine (SNAP), indicate a rapid
68 tigated by using the NO.-generating compound S-nitroso-N-acetylpenicillamine (SNAP), or by stimulatin
70 ntly enhanced TH17 cell differentiation, and S-nitroso-N-acetylpenicillamine (SNAP), the NO donor, do
71 mo-cAMP, nitric oxide (NO), and the NO donor S-nitroso-N-acetylpenicillamine (SNAP), which circumvent
76 NAME, the addition of an exogenous NO donor, S-nitroso-N-acetylpenicillamine (SNAP, 10(-8) M) or an a
77 Whereas a high concentration of the NO donor S-nitroso-N-acetylpenicillamine (SNAP, 100 micromol/L) s
78 0.1 mg/kg i.v., 4 times [group II, n=5]) or S-nitroso-N-acetylpenicillamine (SNAP, 2.5 microg x kg(-
82 -dextran-10K) during suffusion with vehicle, S-nitroso-N-acetylpenicillamine (SNAP; 100 microM) and 3
84 dazole (7NI; 1 mM) or the nitric oxide donor S-nitroso-N-acetylpenicillamine (SNAP; 500 microM-5 mM)
85 of primary cultured RCECs with an NO donor, S-nitroso-N-acetylpenicillamine (SNAP; N-acetyl-3-(nitro
86 s were exposed to combinations of NO donors (S-nitroso-N-acetylpenicillamine [SNAP] and others), a cG
87 nitrosothiol donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine suppressed caspase-9 and
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