| EP1 disruption attenuates end-organ damage in a mouse model of hypertension. | |
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MedLine Citation:
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PMID: 23006735 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Prostaglandin E(2) is a major prostanoid found in the kidney and vasculature contributing to the regulation of blood pressure. The prostaglandin E(2) receptor EP1 has been shown to contribute to hypertension by mediating angiotensin II-dependent vasoconstriction, although its precise role is incompletely characterized. Disruption of the EP1 receptor in C57BL/6J mice reduced the incidence of mortality during severe hypertension induced by uninephrectomy, deoxycorticosterone acetate, and angiotensin II. Mortality was dependent on all components of the model. Death was a result of aortic aneurysm rupture or occurred after development of anasarca, each of which was reduced in EP1-/- mice. Mean arterial pressure was increased in treated EP1+/+ and EP1-/- mice; however, this elevation was significantly lower in EP1-/- mice. Blood pressure reduction via administration of hydralazine phenocopied EP1-/- mice. Thus, reduction in blood pressure by disruption of EP1 reduced incidence of mortality and decreased organ damage, suggesting that EP1 receptor blockade may be a viable target for antihypertensive therapy. |
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Authors:
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Christina S Bartlett; Kelli L Boyd; Raymond C Harris; Roy Zent; Richard M Breyer |
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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; Research Support, U.S. Gov't, Non-P.H.S. Date: 2012-09-24 |
Journal Detail:
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Title: Hypertension Volume: 60 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2012 Nov |
Date Detail:
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Created Date: 2012-10-18 Completed Date: 2013-01-10 Revised Date: 2013-04-16 |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 1184-91 Citation Subset: IM |
Affiliation:
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Department of Pharmacology, Vanderbilt University Medical Center, 1161 21 Ave, Medical Center North # B3214, Nashville, TN 37232-2372, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II Animals Antihypertensive Agents / pharmacology Aortic Aneurysm / genetics*, physiopathology Blood Pressure / drug effects, genetics, physiology Desoxycorticosterone Disease Models, Animal* Female Humans Hydralazine / pharmacology Hypertension / etiology, genetics*, physiopathology Kaplan-Meier Estimate Kidney / metabolism, pathology, physiopathology Male Mice Mice, Inbred C57BL Mice, Knockout Nephrectomy Receptors, Prostaglandin E, EP1 Subtype / deficiency, genetics* |
| Grant Support | |
ID/Acronym/Agency:
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2P01DK065123/DK/NIDDK NIH HHS; DK059637/DK/NIDDK NIH HHS; DK075594/DK/NIDDK NIH HHS; DK37097/DK/NIDDK NIH HHS; DK46205/DK/NIDDK NIH HHS; DK62794/DK/NIDDK NIH HHS; DK9921/DK/NIDDK NIH HHS; P01 DK065123/DK/NIDDK NIH HHS; P30 DK079341/DK/NIDDK NIH HHS; P30DK79341-01/DK/NIDDK NIH HHS; P50GM015431/GM/NIGMS NIH HHS; R01 DK062794/DK/NIDDK NIH HHS; R01 DK075594/DK/NIDDK NIH HHS; U24 DK059637/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antihypertensive Agents; 0/Ptger1 protein, mouse; 0/Receptors, Prostaglandin E, EP1 Subtype; 11128-99-7/Angiotensin II; 64-85-7/Desoxycorticosterone; 86-54-4/Hydralazine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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