| Superoxide modulates myogenic contractions of mouse afferent arterioles. | |
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MedLine Citation:
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PMID: 21859962 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Reactive oxygen species enhance or impair autoregulation. Because superoxide is a vasoconstrictor, we tested the hypothesis that stretch generates superoxide that mediates myogenic responses. Increasing perfusion pressure of mouse isolated perfused renal afferent arterioles from 40 to 80 mm Hg reduced their diameter by 13.3±1.8% (P<0.001) and increased reactive oxygen species (ethidium: dihydroethidium fluorescence) by 9.8±2.3% (P<0.05). Stretch-induced fluorescence was reduced significantly (P<0.05) by incubation with Tempol (3.7±0.8%), pegylated superoxide dismutase (3.2±1.0%), or apocynin (3.5±0.9%) but not by pegylated catalase, L-nitroarginine methylester, or Ca(2+)-free medium, relating it to Ca(2+)-independent vascular superoxide. Compared with vehicle, basal tone and myogenic contractions were reduced significantly (P<0.05) by pegylated superoxide dismutase (5.4±0.8), Tempol (4.1±1.0%), apocynin (1.0±1.3%), and diphenyleneiodinium (3.9±0.9%) but not by pegylated catalase (10.1±1.6%). L-Nitroarginine methylester enhanced basal tone, but neither it (15.8±3.3%) nor endothelial NO synthase knockout (10.2±1.8%) significantly changed myogenic contractions. Tempol had no further effect after superoxide dismutase but remained effective after catalase. H(2)O(2) >50 μmol/L caused contractions but at 25 μmol/L inhibited myogenic responses (7.4±0.8%; P<0.01). In conclusion, increasing the pressure within afferent arterioles led to Ca(2+)-independent increased vascular superoxide production from nicotinamide adenine dinucleotide phosphate oxidase, which enhanced myogenic contractions largely independent of NO, whereas H(2)O(2) impaired pressure-induced contractions but was not implicated in the normal myogenic response. |
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Authors:
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En Yin Lai; Anton Wellstein; William J Welch; Christopher S Wilcox |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2011-08-22 |
Journal Detail:
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Title: Hypertension Volume: 58 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2011 Oct |
Date Detail:
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Created Date: 2011-09-15 Completed Date: 2011-11-08 Revised Date: 2012-02-10 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 650-6 Citation Subset: IM |
Affiliation:
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Division of Nephrology and Hypertension, Georgetown University, Washington, DC 20007, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acetophenones
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pharmacology Animals Antioxidants / pharmacology Arterioles / metabolism* Cyclic N-Oxides / pharmacology Enzyme Inhibitors / pharmacology Kidney / blood supply* Male Mice Mice, Inbred C57BL Mice, Knockout Models, Animal Muscle Contraction / drug effects, physiology* Muscle, Smooth, Vascular / metabolism* NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide / metabolism Nitric Oxide Synthase / antagonists & inhibitors, genetics, metabolism Nitric Oxide Synthase Type III / genetics, metabolism Reactive Oxygen Species / metabolism Spin Labels Superoxide Dismutase / pharmacology Superoxides / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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DK-036079/DK/NIDDK NIH HHS; DK-049870/DK/NIDDK NIH HHS; HL-089583/HL/NHLBI NIH HHS; HL-68686/HL/NHLBI NIH HHS; P01 HL068686-10/HL/NHLBI NIH HHS; R01 DK049870-18/DK/NIDDK NIH HHS; R01 HL089583-04/HL/NHLBI NIH HHS; R01 HL089583-05/HL/NHLBI NIH HHS; R37 DK036079-26/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Acetophenones; 0/Antioxidants; 0/Cyclic N-Oxides; 0/Enzyme Inhibitors; 0/Reactive Oxygen Species; 0/Spin Labels; 10102-43-9/Nitric Oxide; 11062-77-4/Superoxides; 2226-96-2/tempol; 498-02-2/acetovanillone; 50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse; EC 1.15.1.1/Superoxide Dismutase |
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