دورية أكاديمية
أعرض في EDS

Evidence for G-Protein-Coupled Estrogen Receptor as a Pronatriuretic Factor.

التفاصيل البيبلوغرافية
العنوان: Evidence for G-Protein-Coupled Estrogen Receptor as a Pronatriuretic Factor.
المؤلفون: Gohar EY; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Daugherty EM; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Aceves JO; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Sedaka R; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Obi IE; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Allan JM; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Soliman RH; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Jin C; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., De Miguel C; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Lindsey SH; Department of Pharmacology School of Medicine Tulane University New Orleans LA., Pollock JS; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL., Pollock DM; Division of Nephrology Department of Medicine University of Alabama at Birmingham AL.
المصدر: Journal of the American Heart Association [J Am Heart Assoc] 2020 May 18; Vol. 9 (10), pp. e015110. Date of Electronic Publication: 2020 May 10.
نوع المنشور: Comparative Study; Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 101580524 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 2047-9980 (Electronic) Linking ISSN: 20479980 NLM ISO Abbreviation: J Am Heart Assoc Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Oxford : Wiley-Blackwell
مواضيع طبية MeSH: Natriuresis*/drug effects, Kidney Medulla/*metabolism , Receptors, Estrogen/*metabolism , Receptors, G-Protein-Coupled/*metabolism, Animals ; Cyclopentanes/pharmacology ; Endothelin-1/genetics ; Endothelin-1/metabolism ; Estradiol/metabolism ; Estrogens/pharmacology ; Female ; Kidney Medulla/drug effects ; Male ; Mice, Knockout ; Ovariectomy ; Quinolines/pharmacology ; Rats, Sprague-Dawley ; Receptor, Endothelin A/genetics ; Receptor, Endothelin A/metabolism ; Receptor, Endothelin B/genetics ; Receptor, Endothelin B/metabolism ; Receptors, Estrogen/deficiency ; Receptors, Estrogen/genetics ; Receptors, G-Protein-Coupled/agonists ; Receptors, G-Protein-Coupled/deficiency ; Receptors, G-Protein-Coupled/genetics ; Sex Factors ; Signal Transduction
مستخلص: Background The novel estrogen receptor, G-protein-coupled estrogen receptor (GPER), is responsible for rapid estrogen signaling. GPER activation elicits cardiovascular and nephroprotective effects against salt-induced complications, yet there is no direct evidence for GPER control of renal Na + handling. We hypothesized that GPER activation in the renal medulla facilitates Na + excretion. Methods and Results Herein, we show that infusion of the GPER agonist, G1, to the renal medulla increased Na + excretion in female Sprague Dawley rats, but not male rats. We found that GPER mRNA expression and protein abundance were markedly higher in outer medullary tissues from females relative to males. Blockade of GPER in the renal medulla attenuated Na + excretion in females. Given that medullary endothelin 1 is a well-established natriuretic factor that is regulated by sex and sex steroids, we hypothesized that GPER activation promotes natriuresis via an endothelin 1-dependent pathway. To test this mechanism, we determined the effect of medullary infusion of G1 after blockade of endothelin receptors. Dual endothelin receptor subtype A and endothelin receptor subtype B antagonism attenuated G1-induced natriuresis in females. Unlike males, female mice with genetic deletion of GPER had reduced endothelin 1, endothelin receptor subtype A, and endothelin receptor subtype B mRNA expression compared with wild-type controls. More important, we found that systemic GPER activation ameliorates the increase in mean arterial pressure induced by ovariectomy. Conclusions Our data uncover a novel role for renal medullary GPER in promoting Na + excretion via an endothelin 1-dependent pathway in female rats, but not in males. These results highlight GPER as a potential therapeutic target for salt-sensitive hypertension in postmenopausal women.
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معلومات مُعتمدة: T32 HL007918 United States HL NHLBI NIH HHS; R01 HL133619 United States HL NHLBI NIH HHS; R25 DK115353 United States DK NIDDK NIH HHS; P30 DK079626 United States DK NIDDK NIH HHS; F31 DK111067 United States DK NIDDK NIH HHS; K01 HL145324 United States HL NHLBI NIH HHS; K99 DK119413 United States DK NIDDK NIH HHS; P01 HL136267 United States HL NHLBI NIH HHS; P01 HL069999 United States HL NHLBI NIH HHS
فهرسة مساهمة: Keywords: GPER; endothelin 1; estrogen; hypertension; kidney; sodium excretion
المشرفين على المادة: 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 (Endothelin-1)
0 (Estrogens)
0 (GPER1 protein, mouse)
0 (Gper1 protein, rat)
0 (Quinolines)
0 (Receptor, Endothelin A)
0 (Receptor, Endothelin B)
0 (Receptors, Estrogen)
0 (Receptors, G-Protein-Coupled)
4TI98Z838E (Estradiol)
تواريخ الأحداث: Date Created: 20200512 Date Completed: 20210310 Latest Revision: 20240430
رمز التحديث: 20240430
مُعرف محوري في PubMed: PMC7660860
DOI: 10.1161/JAHA.119.015110
PMID: 32390531
قاعدة البيانات: MEDLINE
الوصف
تدمد:2047-9980
DOI:10.1161/JAHA.119.015110