Nitrite reduction and cardiovascular protection.

摘要: Inorganic nitrite, a metabolite of endogenously produced nitric oxide (NO) from NO synthases (NOS), provides the largest endocrine source directly bioavailable NO. The conversion nitrite to occurs mainly through enzymatic reduction, mediated by range proteins, including haem-globins, molybdo-flavoproteins, mitochondrial cytochrome P450 enzymes, and NOS. Such reduction is particularly favoured under hypoxia, when endogenous formation NOS impaired. Under normoxic conditions, majority these reductases also scavenge NO, or diminish its bioavailability via reactive oxygen species (ROS) production, suggesting an intricate balance. Moreover, whether endogenously, derived exogenous nitrate administration (including dietary sources Nitrate-Nitrite-NO pathway) beneficially modulates many key cardiovascular pathological processes. In this review, we highlight landmark studies which revealed nitrite's function in biological systems, inspect evolving role protection. Whilst effects have been ascribed activity one more reductases, discuss newly-identified mechanisms, anhydration, involvement s-nitrosothiols, nitro-fatty acids, direct signalling, involving modification structure function, ROS production. This article part Special Issue entitled "Redox Signalling Cardiovascular System".