The inorganic anions nitrate (NO3-) and nitrite (NO2-) were previously thought to be inert end products of endogenous nitric oxide (NO) metabolism However, recent studies show that these supposedly inert anions can be recycled in vivo to form NO, representing an important alternative source of NO to the classical L-arginine-NO-synthase pathway, in particular in hypoxic states 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

The nitrate–nitrite–nitric oxide pathway in physiology and therapeutics

The control of arterial pressure during sleep was studied in 13 untreated, unsedated subjects aged 20 to 46, including 7 with hypertension. Arterial pressure was measured directly. A transient rise of arterial pressure up to 30 mm Hg was produced by the sudden intravenous injection of 0.25 to 2 µg of angiotensin. Linear plots were obtained in 10 of 13 subjects when the systolic pressures of successive pulses during the pressure rise were plotted against the pulse intervals which began the next beat. The relationship was disturbed by movement or arousal, and was better when pulse intervals falling in inspiration were discarded. The slope of the line (milliseconds of cardiac slowing per millimeter rise in systolic pressure) in the awake subject ranged from 2 to 15.5 msec/mm Hg, and from 4.5 to 28.9 during sleep. Reflex sensitivity was highest in dreaming sleep. In 7 of 10 subjects, baroreflex sensitivity increased significantly during sleep; in 6, the prevailing arterial pressure was inversely correlated wi...

Reflex Regulation of Arterial Pressure during Sleep in Man: A Quantitative Method of Assessing Baroreflex Sensitivity

Quantitative Clinical Chemistry

The effects of sublingual nitroglycerin and inhaled amyl nitrite on the arteriolar and venous beds of the forearm were studied in 11 normal subjects. Forearm blood flow was measured with a strain-gauge plethysmograph, and venous tone was determined both by an acute occlusion technic, and by several equilibration technics. Nitroglycerin reduced systemic arterial pressure, elevated forearm blood flow, lowered forearm vascular resistance and decreased venous tone. Amyl nitrite diminished arterial pressure, elevated forearm blood flow, markedly decreased forearm vascular resistance, but in contrast to nitroglycerin augmented venous tone strikingly. This venoconstriction was abolished or diminished when adrenergic activity was impeded by administration of either guanethidine or reserpine.

The Effects of Nitroglycerin and Amyl Nitrite on Arteriolar and Venous Tone in the Human Forearm

In this review we consider the effects of endogenous and pharmacological levels of nitrite under conditions of hypoxia. In humans, the nitrite anion has long been considered as metastable intermediate in the oxidation of nitric oxide radicals to the stable metabolite nitrate. This oxidation cascade was thought to be irreversible under physiological conditions. However, a growing body of experimental observations attests that the presence of endogenous nitrite regulates a number of signaling events along the physiological and pathophysiological oxygen gradient. Hypoxic signaling events include vasodilation, modulation of mitochondrial respiration, and cytoprotection following ischemic insult. These phenomena are attributed to the reduction of nitrite anions to nitric oxide if local oxygen levels in tissues decrease. Recent research identified a growing list of enzymatic and nonenzymatic pathways for this endogenous reduction of nitrite. Additional direct signaling events not involving free nitric oxide are proposed. We here discuss the mechanisms and properties of these various pathways and the role played by the local concentration of free oxygen in the affected tissue.

/pdf/nitrite-as-regulator-of-hypoxic-signaling-in-mammalian-5dc70ahb8i.pdf

Nitrite as regulator of hypoxic signaling in mammalian physiology

/pdf/the-nature-of-circulatory-collapse-induced-by-sodium-nitrite-l8rgaxuzpo.pdf

The nature of circulatory collapse induced by sodium nitrite.

/pdf/the-role-of-the-venous-system-in-circulatory-collapse-33xhbx6cct.pdf

The role of the venous system in circulatory collapse induced by sodium nitrite.

Myocardial abscess with perforation of the heart

There is increasing evidence that the biological function of vitamin B1 is concerned with oxidative processes in the living organism. In studies of oxygen utilization by manometric methods, Peters and his coworkers (1, 2) have shown that there is increased oxygen uptake by deficient brain and kidney tissues in vitro following the addition of vitamin B1. In the same laboratory Thompson and Johnson (3, 4) found increased amounts of carbonyl compounds in the blood of B1 avitaminotic pigeons and rats. Clinical confirmation has recently been given these experimental findings by Platt and Lu (5), who reported marked increases in the carbonyl compounds in the blood of patients with acute beriberi in the Orient. These authors measured the carbonyl compounds by means of the bisulphite binding power of the blood. Pyruvic acid has received most attention, chiefly through the emphasis given to it by Peters et al. (2). Thompson and Johnson concluded that the major portion of the increase in bisulphite binding substances (B.B.S.) in the blood of pigeons and rats severely deficient in vitamin B1 was due to pyruvic acid. On the other hand, Sherman and Elvehjem (6) found no increase in the B.B.S. in the blood of chickens deficient in vitamin B1, but did find that these birds, in contrast to normal birds, showed a sharp rise in blood B.B.S. after the intravenous injection of sodium pyruvate. Platt and Lu in a recent report (7) state that the increases in B.B.S. in the blood of fulminating cases of beriberi are due mainly to pyruvic acid. For 2 years an investigation has been in progress in this laboratory on patients with symptoms and signs of vitamin B1 deficiency closely resembling those seen in oriental \"wets\" beriberi (8,

/pdf/the-bisulphite-binding-power-of-the-blood-in-health-and-in-3ijidx6o5m.pdf

The bisulphite binding power of the blood in health and in disease, with special reference to vitamin b1 deficiency

Previous studies (1, 2) of vasomotor collapse induced by sodium nitrite in normal subjects in the upright position have revealed that the characteristic symptoms and signs of collapse are manifested by a fall in the arterial pressure, particularly the pulse pressure, as well as in the venous pressure. Further, the collapse is accompanied by an increase in arterial and arteriolar tone, but a decrease in venous tone. The blood flow through the hand is unchanged during the early stage of collapse as a result of compensatory vascular changes; later, however, there is a sharp fall in the blood flow which is followed by syncope. The manifestations and mechanism of this collapse are identical with those seen in disease. Since epinephrin is one of the agents commonly used in the treatment of collapse, it was decided to investigate the mode of action and the therapeutic efficacy of this drug in experimental nitrite collapse. Such a controlled study is of interest, because similar observations are not feasible in collapse occurring in patients who are gravely ill.

/pdf/the-effect-of-epinephrin-in-circulatory-collapse-induced-by-5f918qpw38.pdf

The effect of epinephrin in circulatory collapse induced by sodium nitrite.

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