| Intrarenal renin-angiotensin system and counteracting protective mechanisms in angiotensin II-dependent hypertension. | |
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MedLine Citation:
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PMID: 17444274 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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It is now well accepted that alterations in kidney function, due either to primary renal disease or to inappropriate hormonal influences on the kidney, are a cardinal characteristic in all forms of hypertension, and lead to a reduced ability of the kidneys to excrete sodium and the consequent development of elevated arterial pressures. However, it is also apparent that many extrarenal factors are important contributors to altered kidney function and hypertension. Central to many hypertensinogenic processes is the inappropriate activation of the renin-angiotensin system (RAS) and its downstream consequences by various pathophysiologic mechanisms. There may also be derangements in arachidonic acid metabolites, endothelium derived factors such as nitric oxide and carbon monoxide, and various paracrine and neural systems that normally interact with or provide a counteracting balance to the actions of the RAS. Thus, when the capacity of the kidneys to maintain sodium balance and extracellular fluid volume within appropriate ranges is compromised, increases in arterial pressure become necessary to re-establish normal balance. |
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Authors:
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K D Mitchell; F T Botros; L G Navar |
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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: Acta physiologica Hungarica Volume: 94 ISSN: 0231-424X ISO Abbreviation: Acta Physiol Hung Publication Date: 2007 Mar |
Date Detail:
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Created Date: 2007-04-20 Completed Date: 2007-05-11 Revised Date: 2008-06-11 |
Medline Journal Info:
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Nlm Unique ID: 8309201 Medline TA: Acta Physiol Hung Country: Hungary |
Other Details:
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Languages: eng Pagination: 31-48 Citation Subset: IM |
Affiliation:
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Department of Physiology, Tulane Hypertension and Renal Center of Excellence, Tulane University Health Sciences Center, 1430 Tulane Ave, SL 39, New Orleans, Louisiana, LA 70112, USA. kdmitch@tulane.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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physiology* Animals Atrial Natriuretic Factor / physiology Blood Pressure / physiology Carbon Monoxide / physiology Cyclooxygenase Inhibitors / pharmacology Eicosanoids / biosynthesis Heme / metabolism Heme Oxygenase (Decyclizing) / physiology Hypertension / physiopathology* Hypertension, Renal / etiology Renin-Angiotensin System / physiology* |
| Grant Support | |
ID/Acronym/Agency:
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HL 26371/HL/NHLBI NIH HHS; P20RR017659/RR/NCRR NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cyclooxygenase Inhibitors; 0/Eicosanoids; 11128-99-7/Angiotensin II; 14875-96-8/Heme; 630-08-0/Carbon Monoxide; 85637-73-6/Atrial Natriuretic Factor; EC 1.14.99.3/Heme Oxygenase (Decyclizing) |
| Comments/Corrections | |
Comment In:
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Acta Physiol Hung. 2008 Mar;95(1):127-8; author reply 129-30
[PMID:
18390005
]
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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