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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1999-2-23
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pubmed:abstractText |
Prostaglandins (PGs) are ubiquitous lipid mediators derived from cyclooxygenase metabolism of arachidonic acid that exert a broad range of physiologic activities, including modulation of inflammation, ovulation and arterial blood pressure. PGE2, a chief cyclooxygenase product, modulates blood pressure and fertility, although the specific G protein-coupled receptors mediating these effects remain poorly defined. To evaluate the physiologic role of the PGE2 EP2 receptor subtype, we created mice with targeted disruption of this gene (EP2-/-). EP2-/- mice develop normally but produce small litters and have slightly elevated baseline systolic blood pressure. In EP2-/- mice, the characteristic hypotensive effect of intravenous PGE2 infusion was absent; PGE2 infusion instead produced hypertension. When fed a diet high in salt, the EP2-/- mice developed profound systolic hypertension, whereas wild-type mice showed no change in systolic blood pressure. Analysis of wild-type and EP2-/- mice on day 5 of pregnancy indicated that the reduced litter size of EP2-/- mice is due to a pre-implantation defect. This reduction of implanted embryos could be accounted for by impaired ovulation and dramatic reductions in fertilization observed on day 2 of pregnancy. These data demonstrate that the EP2 receptor mediates arterial dilatation, salt-sensitive hypertension, and also plays an essential part in female fertility.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Ptger2 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Prostaglandin E,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Prostaglandin E, EP2...,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium, Dietary
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1078-8956
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
5
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
217-20
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:9930871-Animals,
pubmed-meshheading:9930871-Blastocyst,
pubmed-meshheading:9930871-Cloning, Molecular,
pubmed-meshheading:9930871-Embryonic Development,
pubmed-meshheading:9930871-Female,
pubmed-meshheading:9930871-Hypertension,
pubmed-meshheading:9930871-Infertility, Female,
pubmed-meshheading:9930871-Male,
pubmed-meshheading:9930871-Mice,
pubmed-meshheading:9930871-Mice, Inbred C57BL,
pubmed-meshheading:9930871-Mice, Knockout,
pubmed-meshheading:9930871-Pregnancy,
pubmed-meshheading:9930871-Receptors, Prostaglandin E,
pubmed-meshheading:9930871-Receptors, Prostaglandin E, EP2 Subtype,
pubmed-meshheading:9930871-Sodium, Dietary,
pubmed-meshheading:9930871-Vasodilation
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pubmed:year |
1999
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pubmed:articleTitle |
Salt-sensitive hypertension and reduced fertility in mice lacking the prostaglandin EP2 receptor.
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pubmed:affiliation |
Department of Medicine, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-2372, USA.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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