Nitric oxide in the human respiratory cycle

McMahon, Timothy J.; Moon, Richard E.; Luschinger, Ben P.; Carraway, Martha Sue; Stone, Anne E.; Stolp, Bryant W.; Gow, Andrew J.; Pawloski, John R.; Watke, Paula; Singel, David J.; Piantadosi, Claude A.; Stamler, Jonathan S.

doi:10.1038/nm718

Cited by 434 publications

(446 citation statements)

References 43 publications

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“…The absence of any arterial-venous difference of NO metabolites in the turtle (Fig.2) differs from humans and rats, where nitrite and RSNO are typically higher on the arterial side of the circulation and reflect the differences in the O 2 -linked generation of products of NO metabolism in the arterial circulation and consumption in the venous circulation (Stamler et al, 1997;Gladwin et al, 2000;McMahon et al, 2002;Cosby et al, 2003). The lower metabolic rate of turtles compared with mammals, reflected by the small arterial-venous gradient in the O 2 content of turtles even in normoxic animals (Fig.1A), may explain the absence of significant arterial-venous gradients in NO metabolites.…”

Section: Basal No Metabolites and Thiols In The Bloodmentioning

confidence: 94%

Circulating nitric oxide metabolites and cardiovascular changes in the turtleTrachemys scriptaduring normoxia, anoxia and reoxygenation

Jacobsen

Hansen

Frank

et al. 2012

Journal of Experimental Biology

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SUMMARYTurtles of the genus Trachemys show a remarkable ability to survive prolonged anoxia. This is achieved by a strong metabolic depression, redistribution of blood flow and high levels of antioxidant defence. To understand whether nitric oxide (NO), a major regulator of vasodilatation and oxygen consumption, may be involved in the adaptive response of Trachemys to anoxia, we measured NO metabolites (nitrite, S-nitroso, Fe-nitrosyl and N-nitroso compounds) in the plasma and red blood cells of venous and arterial blood of Trachemys scripta turtles during normoxia and after anoxia (3h) and reoxygenation (30min) at 21°C, while monitoring blood oxygen content and circulatory parameters. Anoxia caused complete blood oxygen depletion, decrease in heart rate and arterial pressure, and increase in venous pressure, which may enhance heart filling and improve cardiac contractility. Nitrite was present at high, micromolar levels in normoxic blood, as in some other anoxia-tolerant species, without significant arterial-venous differences. Normoxic levels of erythrocyte S-nitroso compounds were within the range found for other vertebrates, despite very high measured thiol content. Fe-nitrosyl and N-nitroso compounds were present at high micromolar levels under normoxia and increased further after anoxia and reoxygenation, suggesting NO generation from nitrite catalysed by deoxygenated haemoglobin, which in turtle had a higher nitrite reductase activity than in hypoxia-intolerant species. Taken together, these data indicate constitutively high circulating levels of NO metabolites and significant increases in blood NO after anoxia and reoxygenation that may contribute to the complex physiological response in the extreme anoxia tolerance of Trachemys turtles.

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Section: Basal No Metabolites and Thiols In The Bloodmentioning

confidence: 94%

Circulating nitric oxide metabolites and cardiovascular changes in the turtleTrachemys scriptaduring normoxia, anoxia and reoxygenation

Jacobsen

Hansen

Frank

et al. 2012

Journal of Experimental Biology

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“…The levels of nitrosylHb in mammalian circulation have been reported to be ~5μM in mixed venous blood and ~2.5μM in arterial blood [32]. When mosquitoes feed, blood is drawn from the peripheral venous circulation, thus the blood meal likely contains nitrosylHb.…”

Section: Possible Mechanisms For Iron Nitrosylhb Formation In the Mosmentioning

confidence: 99%

Nitric oxide metabolites induced in Anopheles stephensi control malaria parasite infection

Peterson

Gow

Luckhart

2007

Free Radical Biology and Medicine

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100

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Malaria parasite infection in anopheline mosquitoes is limited by inflammatory levels of nitric oxide metabolites. To assess the mechanisms of parasite stasis or toxicity, we investigated the biochemistry of these metabolites within the blood-filled mosquito midgut. Our data indicate that nitrates, but not nitrites, are elevated in the Plasmodium-infected midgut. Although levels of S-nitrosothiols do not change with infection, blood proteins are S-nitrosylated after ingestion by the mosquito. In addition, photolyzable nitric oxide, which can be attributed to metal nitrosyls, is elevated following infection and, based on the abundance of hemoglobin, likely includes heme iron nitrosyl. The persistance of oxyhemoglobin throughout blood digestion and changes in hemoglobin conformation in response to infection suggest that hemoglobin catalyzes the synthesis of nitric oxide metabolites in a reducing environment. Provision of urate, a potent reductant and scavenger of oxidants and nitrating agents, as a dietary supplement to mosquitoes increased parasite infection levels relative to allantoin-fed controls, suggesting that nitrosative and/or oxidative stresses negatively impact developing parasites. Collectively, our results reveal a unique role for nitric oxide in an oxyhemoglobin-rich environment. In contrast to facilitating oxygen delivery by hemoglobin in the mammalian vasculature, nitric oxide synthesis in the blood-filled mosquito midgut drives the formation of toxic metabolites that limit parasite development.

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“…30 Stored blood also has lower concentrations of 2,3 diphosphoglycerate, which reduces oxygen delivery to peripheral tissue. 31,32 Transfusions have been reported to be associated with increased levels of proinflammatory mediators such as C-reactive protein, interleukin-6, and bactericidal permeability-increasing protein. 32 Each of these mechanisms might promote peripheral or myocardial ischemia.…”

Section: Consequences Of Transfusionmentioning

confidence: 99%