Document Detail

Renal actions of RGS2 control blood pressure.
MedLine Citation:
PMID:  20847141     Owner:  NLM     Status:  MEDLINE    
G protein-coupled receptors (GPCRs) have key roles in cardiovascular regulation and are important targets for the treatment of hypertension. GTPase-activating proteins, such as RGS2, modulate downstream signaling by GPCRs. RGS2 displays regulatory selectivity for the Gαq subclass of G proteins, and mice lacking RGS2 develop hypertension through incompletely understood mechanisms. Using total body RGS2-deficient mice, we used a kidney crosstransplantation strategy to examine separately the contributions of RGS2 actions in the kidney from those in extrarenal tissues with regard to BP regulation. Loss of renal RGS2 was sufficient to cause hypertension, whereas the absence of RGS2 from all extrarenal tissues including the peripheral vasculature did not significantly alter BP. Accordingly, these results suggest that RGS2 acts within the kidney to modulate BP and prevent hypertension. These data support a critical role for the renal epithelium and/or vasculature as the final determinants of the intra-arterial pressure in hypertension.
Susan B Gurley; Robert C Griffiths; Michael E Mendelsohn; Richard H Karas; 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:  2010-09-16
Journal Detail:
Title:  Journal of the American Society of Nephrology : JASN     Volume:  21     ISSN:  1533-3450     ISO Abbreviation:  J. Am. Soc. Nephrol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-01     Completed Date:  2010-11-22     Revised Date:  2013-05-27    
Medline Journal Info:
Nlm Unique ID:  9013836     Medline TA:  J Am Soc Nephrol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1847-51     Citation Subset:  IM    
Department of Medicine, Division of Nephrology, Duke University Medical Center, Durham, NC 27710, USA.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Blood Pressure / physiology*
Disease Models, Animal
Hypertension / physiopathology
Kidney / physiology*
Kidney Transplantation / physiology
Mice, Knockout
RGS Proteins / genetics,  physiology*
Receptors, G-Protein-Coupled / physiology
Grant Support
Reg. No./Substance:
0/RGS Proteins; 0/Receptors, G-Protein-Coupled; 0/Rgs2 protein, mouse
Comment In:
J Am Soc Nephrol. 2010 Nov;21(11):1809-10   [PMID:  20947628 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Fibroblast expression of an I?B dominant-negative transgene attenuates renal fibrosis.
Next Document:  Low socioeconomic status associates with higher serum phosphate irrespective of race.