| Attenuation of salt-induced cardiac remodeling and diastolic dysfunction by the GPER agonist G-1 in female mRen2.Lewis rats. | |
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MedLine Citation:
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PMID: 21082029 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Jewell A Jessup; Sarah H Lindsey; Hao Wang; Mark C Chappell; Leanne Groban |
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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 Date: 2010-11-03 |
Journal Detail:
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Title: PloS one Volume: 5 ISSN: 1932-6203 ISO Abbreviation: PLoS ONE Publication Date: 2010 |
Date Detail:
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Created Date: 2010-11-18 Completed Date: 2011-04-27 Revised Date: 2012-11-16 |
Medline Journal Info:
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Nlm Unique ID: 101285081 Medline TA: PLoS One Country: United States |
Other Details:
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Languages: eng Pagination: e15433 Citation Subset: IM |
Affiliation:
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The Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston Salem, North Carolina, United States of America. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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:
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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 |
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