| Role of nitric oxide in cardiovascular adaptation to intermittent hypoxia. | |
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MedLine Citation:
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PMID: 16565431 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Hypoxia is one of the most frequently encountered stresses in health and disease. The duration, frequency, and severity of hypoxic episodes are critical factors determining whether hypoxia is beneficial or harmful. Adaptation to intermittent hypoxia has been demonstrated to confer cardiovascular protection against more severe and sustained hypoxia, and, moreover, to protect against other stresses, including ischemia. Thus, the direct and cross protective effects of adaptation to intermittent hypoxia have been used for treatment and prevention of a variety of diseases and to increase efficiency of exercise training. Evidence is mounting that nitric oxide (NO) plays a central role in these adaptive mechanisms. NO-dependent protective mechanisms activated by intermittent hypoxia include stimulation of NO synthesis as well as restriction of NO overproduction. In addition, alternative, nonenzymic sources of NO and negative feedback of NO synthesis are important factors in optimizing NO concentrations. The adaptive enhancement of NO synthesis and/or availability activates or increases expression of other protective factors, including heat shock proteins, antioxidants and prostaglandins, making the protection more robust and sustained. Understanding the role of NO in mechanisms of adaptation to hypoxia will support development of therapies to prevent and treat hypoxic or ischemic damage to organs and cells and to increase adaptive capabilities of the organism. |
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Authors:
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Eugenia B Manukhina; H Fred Downey; Robert T Mallet |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review |
Journal Detail:
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Title: Experimental biology and medicine (Maywood, N.J.) Volume: 231 ISSN: 1535-3702 ISO Abbreviation: Exp. Biol. Med. (Maywood) Publication Date: 2006 Apr |
Date Detail:
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Created Date: 2006-03-27 Completed Date: 2006-04-21 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100973463 Medline TA: Exp Biol Med (Maywood) Country: United States |
Other Details:
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Languages: eng Pagination: 343-65 Citation Subset: IM |
Affiliation:
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Institute of General Pathology and Pathophysiology, Moscow, Russia. manukh@orc.ru |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptation, Physiological Animals Anoxia / metabolism* Calcium / metabolism Cardiovascular System / metabolism* Heat-Shock Proteins / metabolism Humans Nitric Oxide / metabolism* Nitric Oxide Synthase / metabolism Oxygen / metabolism Protective Agents Vasodilation |
| Grant Support | |
ID/Acronym/Agency:
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R01 HL-064785/HL/NHLBI NIH HHS; R01 HL-071684/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Heat-Shock Proteins; 0/Protective Agents; 10102-43-9/Nitric Oxide; 7440-70-2/Calcium; 7782-44-7/Oxygen; EC 1.14.13.39/Nitric Oxide Synthase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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