Crawford 2006 Blood: Difference between revisions
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{{Publication | {{Publication | ||
|title=Crawford JH, Isbell TS, Huang Z, Shiva S, Chacko BK, Schechter AN, Darley-Usmar VM, Kerby JD, Lang JD Jr, Kraus D, Ho C, Gladwin MT, Patel RP (2006) Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation. Blood 107:566-74. | |title=Crawford JH, Isbell TS, Huang Z, Shiva S, Chacko BK, Schechter AN, Darley-Usmar VM, Kerby JD, Lang JD Jr, Kraus D, Ho C, Gladwin MT, Patel RP (2006) Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation. Blood 107:566-74. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/16195332 PMID:16195332 ] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/16195332 PMID: 16195332 Open Access] | ||
|authors=Crawford JH, Isbell TS, Huang | |authors=Crawford JH, Isbell TS, Huang Zhi, Shiva S, Chacko BK, Schechter AN, Darley-Usmar VM, Kerby JD, Lang JD Jr, Kraus D, Ho C, Gladwin MT, Patel RP | ||
|year=2006 | |year=2006 | ||
|journal=Blood | |journal=Blood | ||
| Line 16: | Line 16: | ||
|tissues=Blood cells | |tissues=Blood cells | ||
|preparations=Isolated mitochondria | |preparations=Isolated mitochondria | ||
|injuries= | |injuries=Ischemia-reperfusion, Oxidative stress;RONS | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Biomedicine | |discipline=Biomedicine | ||
}} | }} | ||
Latest revision as of 08:52, 17 August 2022
| Crawford JH, Isbell TS, Huang Z, Shiva S, Chacko BK, Schechter AN, Darley-Usmar VM, Kerby JD, Lang JD Jr, Kraus D, Ho C, Gladwin MT, Patel RP (2006) Hypoxia, red blood cells, and nitrite regulate NO-dependent hypoxic vasodilation. Blood 107:566-74. |
Crawford JH, Isbell TS, Huang Zhi, Shiva S, Chacko BK, Schechter AN, Darley-Usmar VM, Kerby JD, Lang JD Jr, Kraus D, Ho C, Gladwin MT, Patel RP (2006) Blood
Abstract: Local vasodilation in response to hypoxia is a fundamental physiologic response ensuring oxygen delivery to tissues under metabolic stress. Recent studies identify a role for the red blood cell (RBC), with hemoglobin the hypoxic sensor. Herein, we investigate the mechanisms regulating this process and explore the relative roles of adenosine triphosphate, S-nitrosohemoglobin, and nitrite as effectors. We provide evidence that hypoxic RBCs mediate vasodilation by reducing nitrite to nitric oxide (NO) and ATP release. NO dependence for nitrite-mediated vasodilation was evidenced by NO gas formation, stimulation of cGMP production, and inhibition of mitochondrial respiration in a process sensitive to the NO scavenger C-PTIO. The nitrite reductase activity of hemoglobin is modulated by heme deoxygenation and heme redox potential, with maximal activity observed at 50% hemoglobin oxygenation (p50). Concomitantly, vasodilation is initiated at the p50, suggesting that oxygen sensing by hemoglobin is mechanistically linked to nitrite reduction and stimulation ofvasodilation. Mutation of the conserved Ξ²93cys residue decreases the heme redox potential (ie, decreases E1/2), an effect that increases nitrite reductase activity and vasodilation at any given hemoglobin saturation. These data support a function for RBC hemoglobin as an allosterically and redox-regulated nitrite reductase whose βenzyme activityβ couples hypoxia to increased NO-dependent blood flow.
β’ O2k-Network Lab: US AL Birmingham Kraus DW
Labels: MiParea: Respiration, Genetic knockout;overexpression
Stress:Ischemia-reperfusion, Oxidative stress;RONS Organism: Rat Tissue;cell: Blood cells Preparation: Isolated mitochondria
HRR: Oxygraph-2k
