Share This Author
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.
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.
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.
Deconstructing sickle cell disease: reappraisal of the role of hemolysis in the development of clinical subphenotypes.
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.
Cell-free hemoglobin limits nitric oxide bioavailability in sickle-cell disease
It is demonstrated here that plasma from patients with sickle-cell disease contains cell-free ferrous hemoglobin, which stoichiometrically consumes micromolar quantities of nitric oxide and abrogates forearm blood flow responses to Nitric oxide donor infusions.
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.
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.
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.