Document Detail


Attenuation of salt-induced cardiac remodeling and diastolic dysfunction by the GPER agonist G-1 in female mRen2.Lewis rats.
MedLine Citation:
PMID:  21082029     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
INTRODUCTION: The G protein-coupled estrogen receptor (GPER) is expressed in various tissues including the heart. Since the mRen2.Lewis strain exhibits salt-dependent hypertension and early diastolic dysfunction, we assessed the effects of the GPER agonist (G-1, 40 nmol/kg/hr for 14 days) or vehicle (VEH, DMSO/EtOH) on cardiac function and structure.
METHODS: Intact female mRen2.Lewis rats were fed a normal salt (0.5% sodium; NS) diet or a high salt (4% sodium; HS) diet for 10 weeks beginning at 5 weeks of age.
RESULTS: Prolonged intake of HS in mRen2.Lewis females resulted in significantly increased blood pressure, mildly reduced systolic function, and left ventricular (LV) diastolic compliance (as signified by a reduced E deceleration time and E deceleration slope), increased relative wall thickness, myocyte size, and mid-myocardial interstitial and perivascular fibrosis. G-1 administration attenuated wall thickness and myocyte hypertrophy, with nominal effects on blood pressure, LV systolic function, LV compliance and cardiac fibrosis in the HS group. G-1 treatment significantly increased LV lusitropy [early mitral annular descent (e')] independent of prevailing salt, and improved the e'/a' ratio in HS versus NS rats (P<0.05) as determined by tissue Doppler.
CONCLUSION: Activation of GPER improved myocardial relaxation in the hypertensive female mRen2.Lewis rat and reduced cardiac myocyte hypertrophy and wall thickness in those rats fed a high salt diet. Moreover, these advantageous effects of the GPER agonist on ventricular lusitropy and remodeling do not appear to be associated with overt changes in blood pressure.
Authors:
Jewell A Jessup; Sarah H Lindsey; Hao Wang; Mark C Chappell; Leanne Groban
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2010-11-03
Journal Detail:
Title:  PloS one     Volume:  5     ISSN:  1932-6203     ISO Abbreviation:  PLoS ONE     Publication Date:  2010  
Date Detail:
Created Date:  2010-11-18     Completed Date:  2011-04-27     Revised Date:  2013-07-03    
Medline Journal Info:
Nlm Unique ID:  101285081     Medline TA:  PLoS One     Country:  United States    
Other Details:
Languages:  eng     Pagination:  e15433     Citation Subset:  IM    
Affiliation:
The Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston Salem, North Carolina, United States of America.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blood Pressure / drug effects*
Cardiomegaly / etiology,  metabolism,  physiopathology
Cyclopentanes / pharmacology*
Diastole
Echocardiography
Female
Heart / drug effects,  physiopathology
Hypertension / etiology,  physiopathology,  prevention & control*
Immunohistochemistry
Mice
Myocardium / metabolism,  pathology
Quinolines / pharmacology*
Rats
Rats, Inbred Lew
Rats, Transgenic
Receptors, G-Protein-Coupled / agonists*,  genetics,  metabolism
Renin / genetics
Reverse Transcriptase Polymerase Chain Reaction
Sodium Chloride, Dietary / administration & dosage
Grant Support
ID/Acronym/Agency:
HL-56973/HL/NHLBI NIH HHS; K08-AG026764-05/AG/NIA NIH HHS; R01 AG033727/AG/NIA NIH HHS; R01 AG033727-02/AG/NIA NIH HHS; R01-AG033727-01/AG/NIA NIH HHS
Chemical
Reg. No./Substance:
0/1-(4-(6-bromobenzo(1,3)dioxol-5-yl)-3a,4,5,9b-tetrahydro-3H-cyclopenta(c)quinolin-8-yl)ethanone; 0/Cyclopentanes; 0/Quinolines; 0/Receptors, G-Protein-Coupled; 0/Ren2 protein, mouse; 0/Sodium Chloride, Dietary; EC 3.4.23.15/Renin
Comments/Corrections

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


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