GSNO 是一种外源性的 NO 供体，是大鼠酒精脱氢酶III类同工酶的底物，能够减少脑血管紧张素II依赖性及非依赖型的 AT1 受体反应。

GSNO is an endogenous transnitrosation donor involved in S-nitrosation of a variety of cellular proteins. GSNO, an exogenous NO donor and substrate of rat alcohol dehydrogenase class III isoenzyme, inhibits cerebral angiotensin II-dependent and -independent AT1 receptor responses.

GSNO completely abolished the AngII-dependent AT1 receptor-mediated vasoconstriction of cerebral arteries. GSNO had no impact on responses to other vasoconstrictors sharing (phenylephrine, U46619) or not (5-HT) the same signalling pathway[1].

Elevated blood pressure, proteinuria, and intrauterine growth restriction associated with PE were induced in Sprague-Dawley rats using L-NAME. These were partially reversed with the use of GSNO[3].

57564-91-7

C10H16N4O7S

336.31

S-亚硝基谷胱甘肽;SNOG;S-Nitrosoglutathione;Glutathione thionitrite;GSNO

DMSO:Soluble
H2O:20 mg/ml(59.47 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years