| Role of AT₁ receptor-mediated salt retention in angiotensin II-dependent hypertension. | |
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MedLine Citation:
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PMID: 21849491 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Activation of type 1 angiotensin II (AT(1)) receptors in the kidney promotes blood pressure elevation and target organ damage, but whether renal AT(1) receptors influence the level of hypertension by stimulating sodium retention or by raising systemic vascular resistance has not been established. In the current studies, we used a kidney cross-transplantation strategy to determine whether increased sodium reabsorption by AT(1) receptors in the kidney mediates the chronic hypertensive response to angiotensin II. We found this to be true. In addition, we also identified a second, nontrivial component of blood pressure elevation induced by activation of renal AT(1) receptors that is sodium-independent. As the kidney has the capacity to limit the transmission of elevated systemic blood pressure into the renal microcirculation, prior studies struggled to clearly discriminate the relative contributions of blood pressure elevation vs. activation of AT(1) receptors to hypertensive kidney injury. In our model, we found that rapid surges in blood pressure, which may overcome the kidney's capacity to prevent perturbations in renal hemodynamics, correlate closely with kidney damage in hypertension. Moreover, maximal kidney injury in hypertension may require activation of a pool of nonrenal, systemic AT(1) receptors. These studies provide insight into precise mechanisms through which AT(1) receptor blockade influences the progression of hypertensive kidney disease. |
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Authors:
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Steven D Crowley; Jiandong Zhang; Maria Herrera; Robert Griffiths; Phillip Ruiz; Thomas M Coffman |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S. Date: 2011-08-17 |
Journal Detail:
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Title: American journal of physiology. Renal physiology Volume: 301 ISSN: 1522-1466 ISO Abbreviation: Am. J. Physiol. Renal Physiol. Publication Date: 2011 Nov |
Date Detail:
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Created Date: 2011-11-01 Completed Date: 2011-12-12 Revised Date: 2013-02-19 |
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: F1124-30 Citation Subset: IM |
Affiliation:
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Division of Nephrology, Department of Medicine, Duke University Medical Center and Durham Veterans Affairs Medical Center, Durham, North Carolina, USA. crowl004@mc.duke.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Albuminuria
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metabolism Angiotensin II / pharmacology* Animals Blood Pressure / physiology Cardiomegaly / prevention & control Diet, Sodium-Restricted Disease Progression Hypertension, Renal / chemically induced, metabolism*, pathology Kidney / pathology, physiology Kidney Transplantation / physiology Male Mice Mice, 129 Strain Mice, Inbred C57BL Mineralocorticoid Receptor Antagonists / pharmacology Receptor, Angiotensin, Type 1 / physiology* Salts / metabolism* |
| Grant Support | |
ID/Acronym/Agency:
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DK087893-01/DK/NIDDK NIH HHS; R01 DK087893/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Mineralocorticoid Receptor Antagonists; 0/Receptor, Angiotensin, Type 1; 0/Salts; 11128-99-7/Angiotensin II |
| Comments/Corrections | |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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