| Cerebral microvascular dilation during hypotension and decreased oxygen tension: a role for nNOS. | |
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MedLine Citation:
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PMID: 17630350 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Endothelial (eNOS) and neuronal nitric oxide synthase (nNOS) are implicated as important contributors to cerebral vascular regulation through nitric oxide (NO). However, direct in vivo measurements of NO in the brain have not been used to dissect their relative roles, particularly as related to oxygenation of brain tissue. We found that, in vivo, rat cerebral arterioles had increased NO concentration ([NO]) and diameter at reduced periarteriolar oxygen tension (Po(2)) when either bath oxygen tension or arterial pressure was decreased. Using these protocols with highly selective blockade of nNOS, we tested the hypothesis that brain tissue nNOS could donate NO to the arterioles at rest and during periods of reduced perivascular oxygen tension, such as during hypotension or reduced local availability of oxygen. The decline in periarteriolar Po(2) by bath manipulation increased [NO] and vessel diameter comparable with responses at similarly decreased Po(2) during hypotension. To determine whether the nNOS provided much of the vascular wall NO, nNOS was locally suppressed with the highly selective inhibitor N-(4S)-(4-amino-5-[aminoethyl]aminopentyl)-N'-nitroguanidine. After blockade, resting [NO], Po(2), and diameters decreased, and the increase in [NO] during reduced Po(2) or hypotension was completely absent. However, flow-mediated dilation during occlusion of a collateral arteriole did remain intact after nNOS blockade and the vessel wall [NO] increased to approximately 80% of normal. Therefore, nNOS predominantly increased NO during decreased periarteriolar oxygen tension, such as that during hypotension, but eNOS was the dominant source of NO for flow shear mechanisms. |
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Authors:
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Holly D Bauser-Heaton; H Glenn Bohlen |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2007-07-13 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 293 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2007 Oct |
Date Detail:
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Created Date: 2007-10-09 Completed Date: 2007-11-21 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H2193-201 Citation Subset: IM |
Affiliation:
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Department of Cellular and Integrative Physiology, Indiana University Medical School, Indianapolis, Indiana 46202, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arterioles / physiopathology Cerebral Cortex* / blood supply, drug effects, enzymology, metabolism Cerebrovascular Circulation* / drug effects Disease Models, Animal Electrodes, Implanted Endothelium, Vascular / enzymology, metabolism Enzyme Inhibitors / pharmacology Glutamic Acid / metabolism Guanidines / pharmacology Hemorrhage / complications, metabolism, physiopathology Hypotension / enzymology, etiology, metabolism, physiopathology* Male Microelectrodes NG-Nitroarginine Methyl Ester / pharmacology Neurons / drug effects, enzymology, metabolism* Nitric Oxide / metabolism* Nitric Oxide Synthase / antagonists & inhibitors, metabolism* Nitric Oxide Synthase Type III / antagonists & inhibitors, metabolism Nitro Compounds / pharmacology Oxygen / blood* Rats Rats, Sprague-Dawley Vasodilation* / drug effects |
| Grant Support | |
ID/Acronym/Agency:
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HL-20605/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 0/Guanidines; 0/N-(4-amino-5-(aminoethyl)aminopentyl)-N'-nitroguanidine; 0/Nitro Compounds; 10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; 56-86-0/Glutamic Acid; 7782-44-7/Oxygen; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos1 protein, rat; EC 1.14.13.39/Nos3 protein, rat |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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