S-Nitrosothiols as potential therapeutics to induce a mobilizable vascular store of nitric oxide to counteract endothelial dysfunction

H2S- and NO-releasing gasotransmitter platform: A crosstalk signaling pathway in the treatment of acute kidney injury

“…Thus, small RSNOs such as GSNO may transfer the NO group from one thiol to another (S—NO → protein thiols), leading to S-nitrosated proteins, which is a mechanism dependent on the cell’s surrounding chemical environment [ 93 ]. GSNO is an endogenous molecule that increases NO bioavailability and has NO-like activity, such as vasodilation [ 94 ], anti-oxidant effects [ 95 ], tissue repair [ 96 , 97 ], anti-microbial activity [ 98 , 99 ], among others. GSNO (50 μg/kg body weight) has shown renoprotective effects on the treatment of sepsis-induced AKI applied to rat models with lipopolysaccharide-induced sepsis [ 100 ].…”

The Mechanisms of Restenosis and Relevance to Next Generation Stent Design

“…These molecules are called NO donors due to their ability to enzymatically break down and release NO into the surrounding tissue. These NO donors can be synthesised endogenously, with some, such as S-nitrosoglutathione (GSNO), reported to enable NO storage in the vascular wall [63,64]. Similarly, synthetic RSNOs such as S-nitroso-N-acetyl-penicillamine (SNAP) have also been demonstrated to provide a depot of NO in the vascular wall along with the ability to catalytically generate NO [63][64][65] (refer to Table 1).…”

“…These NO donors can be synthesised endogenously, with some, such as S-nitrosoglutathione (GSNO), reported to enable NO storage in the vascular wall [63,64]. Similarly, synthetic RSNOs such as S-nitroso-N-acetyl-penicillamine (SNAP) have also been demonstrated to provide a depot of NO in the vascular wall along with the ability to catalytically generate NO [63][64][65] (refer to Table 1). Due to these properties, NO donors such as SNAP and S-nitroso-N-acetylcysteine (NACNO) are currently undergoing investigation to determine if they could be used therapeutically to treat endothelial dysfunction [63] and may additionally function to limit restenosis post PCI.…”

A physiologically relevant role for NO stored in vascular smooth muscle cells: A novel theory of vascular NO signaling

“…For example, exposure of isolated arteries to compounds that deplete SNOs attenuates both light- and thiol-mediated relaxation [ 86 , [93] , [94] , [95] ]. Conversely, incubating vessels with membrane-permeable SNOs to increase concentrations of NO adducts in the vessel wall augments thiol-mediated relaxation [ 96 ]. In addition, exposure of arteries to red light stimulates the release of a vasodilator with characteristics of SNOs from the vessel [ 84 ], highlighting the close relation of SNOs to the intracellular NO store.…”