Role of the red blood cell in nitric oxide homeostasis and hypoxic vasodilation.

摘要: Nitric oxide (NO) regulates normal vasomotor tone and modulates important homeostatic functions such as thrombosis, cellular proliferation, adhesion molecule expression. Recent data implicate a critical function for hemoglobin the erythrocyte in regulating bioavailability of NO vascular compartment. Under normoxic conditions erythrocytic scavenges produces vasopressor effect that is limited by diffusional barriers along endothelium unstirred layer around erythrocyte. In hemolytic diseases, intravascular hemolysis releases from red blood cell into plasma (decompartmentalizes hemoglobin), which then able to scavenge endothelial derived 600-fold faster than hemoglobin, thereby dysregulating homoestasis. addition releasing contains arginase when released further dysregulates arginine metabolism. These support existence novel mechanism human disease, associated dysfunction, potentially participates vasculopathy iatrogenic hereditary conditions. providing an scavenging role physiological regulation NO-dependent vasodilation, may deliver deoxygenates. Two mechanisms have been proposed explain this principle: 1) Oxygen linked allosteric delivery S-nitrosothiols S-nitrosated (SNO-Hb), 2) nitrite reductase activity deoxygenated reduces vasodilates circulation oxygen gradient. The later newly described discussed context hypoxic flow sensing.