glutathione sjogren's syndrome Oxidative stress in autoimmune rheumatic diseases Oxidative-Stress-Associated Molecular Signatures in Immune-Mediated

PMID: 121 HuangPL

Nitrates such as nitroglycerin (NTG) are enzymatically broken down in the vascular wall by both glutathione S-transferase (GST) and mitochondrial aldehyde dehydrogenase isoform 2 (MtADH2) to release the vasodilator substance nitric oxide (NO)(Figure 6)(Zhang et al, 2009) Enzymatic conversion of NTG to NO is greater in venous smooth muscle compared to arterial smooth muscle, which may account for the venoselectivity of NTG at low doses (Bauer & Fung, 1999) Venodilation results in decreased preload (decreased ventricular chamber size, end diastolic volume, fiber tension) = decreased work by the heart Decreased preload & work of the heart results in decreased O , an effect which reduces ischemia (Figure 1) 2 demand Reduction of afterload (arterial resistance), a desirable therapeutic effect produced at higher doses can also produce reflex tachycardia (an unwanted side effect) Other possible contributors to the mechanism of action for nitroglycerin are under investigation, and include: Redistribution of Coronary Blood Flow Nitrates can selectively increase collateral blood flow to ischemic areas (e.g

These data were in line with the hypothesis that neuromuscular junctions, which are the synapses between MNs and muscle fiber, could represent the starting site of MN dysfunction in ALS [269]

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