| Luminal flow regulates NO and O2(-) along the nephron. | |
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MedLine Citation:
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PMID: 21345976 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Urinary flow is not constant but in fact highly variable, altering the mechanical forces (shear stress, stretch, and pressure) exerted on the epithelial cells of the nephron as well as solute delivery. Nitric oxide (NO) and superoxide (O(2)(-)) play important roles in various processes within the kidney. Reductions in NO and increases in O(2)(-) lead to abnormal NaCl and water absorption and hypertension. In the last few years, luminal flow has been shown to be a regulator of NO and O(2)(-) production along the nephron. Increases in luminal flow enhance fluid, Na, and bicarbonate transport in the proximal tubule. However, we know of no reports directly addressing flow regulation of NO and O(2)(-) in this segment. In the thick ascending limb, flow-stimulated NO and O(2)(-) formation has been extensively studied. Luminal flow stimulates NO production by nitric oxide synthase type 3 and its translocation to the apical membrane in medullary thick ascending limbs. These effects are mediated by flow-induced shear stress. In contrast, flow-induced stretch and NaCl delivery stimulate O(2)(-) production by NADPH oxidase in this segment. The interaction between flow-induced NO and O(2)(-) is complex and involves more than one simply scavenging the other. Flow-induced NO prevents flow from increasing O(2)(-) production via cGMP-dependent protein kinase in thick ascending limbs. In macula densa cells, shear stress increases NO production and this requires that the primary cilia be intact. The role of luminal flow in NO and O(2)(-) production in the distal tubule is not known. In cultured inner medullary collecting duct cells, shear stress enhances nitrite accumulation, a measure of NO production. Although much progress has been made on this subject in the last few years, there are still many unanswered questions. |
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Authors:
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Pablo D Cabral; Jeffrey L Garvin |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Review Date: 2011-02-23 |
Journal Detail:
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Title: American journal of physiology. Renal physiology Volume: 300 ISSN: 1522-1466 ISO Abbreviation: Am. J. Physiol. Renal Physiol. Publication Date: 2011 May |
Date Detail:
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Created Date: 2011-05-05 Completed Date: 2011-07-01 Revised Date: 2012-05-01 |
Medline Journal Info:
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Nlm Unique ID: 100901990 Medline TA: Am J Physiol Renal Physiol Country: United States |
Other Details:
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Languages: eng Pagination: F1047-53 Citation Subset: IM |
Affiliation:
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Hypertension and Vascular Research Div., Dept. of Internal Medicine, Henry Ford Hospital, Detroit, MI 48202, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Humans Mechanotransduction, Cellular* NADPH Oxidase / metabolism Nephrons / metabolism* Nitric Oxide / metabolism* Nitric Oxide Synthase Type III / metabolism Pressure Sodium Chloride, Dietary / metabolism Stress, Mechanical Superoxides / metabolism* Urodynamics* |
| Grant Support | |
ID/Acronym/Agency:
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HL 028982/HL/NHLBI NIH HHS; HL 070985/HL/NHLBI NIH HHS; HL 090550/HL/NHLBI NIH HHS; R01 HL070985-10/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Sodium Chloride, Dietary; 10102-43-9/Nitric Oxide; 11062-77-4/Superoxides; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.6.3.1/NADPH Oxidase |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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