Document Detail


Role of AT₁ receptor-mediated salt retention in angiotensin II-dependent hypertension.
MedLine Citation:
PMID:  21849491     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Steven D Crowley; Jiandong Zhang; Maria Herrera; Robert Griffiths; Phillip Ruiz; Thomas M Coffman
Publication Detail:
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:
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:
Created Date:  2011-11-01     Completed Date:  2011-12-12     Revised Date:  2013-06-28    
Medline Journal Info:
Nlm Unique ID:  100901990     Medline TA:  Am J Physiol Renal Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  F1124-30     Citation Subset:  IM    
Affiliation:
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:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Albuminuria / 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:
DK087893-01/DK/NIDDK NIH HHS; R01 DK087893/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
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


Previous Document:  Preactivation of AMPK by metformin may ameliorate the epithelial cell damage caused by renal ischemi...
Next Document:  Modulation of outer medullary NaCl transport and oxygenation by nitric oxide and superoxide.