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The nitrate–nitrite–nitric oxide pathway in physiology and therapeutics
This Review discusses the emerging important biological functions of the nitrate–nitrite–NO pathway, and highlights studies that implicate the therapeutic potential of nitrate and nitrite in conditions such as myocardial infarction, stroke, systemic and pulmonary hypertension, and gastric ulceration. Expand
Nitrite reduction to nitric oxide by deoxyhemoglobin vasodilates the human circulation
It is suggested that nitrite represents a major bioavailable pool of NO, and a new physiological function for hemoglobin as a nitrite reductase is described, potentially contributing to hypoxic vasodilation. Expand
Deconstructing sickle cell disease: reappraisal of the role of hemolysis in the development of clinical subphenotypes.
Hemolysis plays less of a role in the vaso-occlusive-viscosity complications of disease like the acute painful episode, osteonecrosis of bone and the acute chest syndrome, and agents that decrease hemolysis or restore NO bioavailability or responsiveness may have potential to reduce the incidence and severity of the hemolytic subphenotypes of sickle cell disease. Expand
The clinical sequelae of intravascular hemolysis and extracellular plasma hemoglobin: a novel mechanism of human disease.
A growing body of evidence supports the existence of a novel mechanism of human disease, namely, hemolysis-associated smooth muscle dystonia, vasculopathy, and endothelial dysfunction. Expand
Sickle-cell disease
More work is needed to develop effective treatments that specifically target pathophysiological changes and clinical complications of sickle-cell disease. Expand
Right ventricular function and failure: report of a National Heart, Lung, and Blood Institute working group on cellular and molecular mechanisms of right heart failure.
A working group charged with delineating in broad terms the current base of scientific and medical understanding about the right ventricle and identifying avenues of investigation likely to meaningfully advance knowledge in a clinically useful direction is convened. Expand
Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease.
Although the deleterious vasoconstrictive effects of cell-free, hemoglobin-based blood substitutes have been appreciated, the systemic effects of chronic hemolysis on nitric oxide bioavailabilityExpand
Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver.
The results suggest that nitrite is a biological storage reserve of NO subserving a critical function in tissue protection from ischemic injury and an unexpected and novel therapy for diseases such as myocardial infarction, organ preservation and transplantation, and shock states. Expand
Deoxymyoglobin Is a Nitrite Reductase That Generates Nitric Oxide and Regulates Mitochondrial Respiration
The nitrite reductase activity of deoxymyoglobin is characterized, which reduces nitrite approximately 36 times faster than deoxyhemoglobin because of its lower heme redox potential, and it is demonstrated that NO generation from nitrite reduction can escape heme autocapture to regulate NO-dependent signaling. Expand
Nitrite augments tolerance to ischemia/reperfusion injury via the modulation of mitochondrial electron transfer
It is reported that both acute and delayed exposure to physiological concentrations of nitrite, given both systemically or orally, potently limits cardiac and hepatic reperfusion injury and may represent an effector of the cell-survival program of ischemic preconditioning and the Mediterranean diet. Expand