Intermittent hypoxia-induced cardio-and vasoprotection: Role of no stores

Nitric oxide (NO) is a highly reactive substance with a short lifetime in the free state. Within the bloodstream and tissues, NO can be bound into complexes which stabilize the molecule, facilitating its transport and intracellular storage. The major biological forms of these NO stores include S-nitrosothiols and dinitrosyl iron complexes, which are capable of exchanging NO. Recent observations in animals and humans have greatly increased interest in possible functions of nitrite as an NO source, especially with respect of its conversion to NO under hypoxic conditions. The NO stores formed by these compounds, on the one hand, provide for protection by sequestering excess free NO after its overproduction and, on the other hand, can be an additional NO source when it is deficient. Intermittent hypoxia may confer protection of the cardiovascular system in the setting of both NO deficiency and NO overproduction. Adaptation of mammals to intermittent hypoxia is associated with formation of NO stores. Thus, formation and degradation of NO stores can play an important role in prevention of cardiovascular disorders associated with either excess or deficiency of NO, and modulation of NO storage, e.g. by intermittent hypoxia conditioning, can be clinically important.