Source:http://linkedlifedata.com/resource/pubmed/id/12574101
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
2
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| pubmed:dateCreated |
2003-2-7
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| pubmed:abstractText |
Recently, the concept of local renin-angiotensin systems (RAS) capable of generating angiotensin II apart from the circulation has received considerable attention. To investigate this, we generated ACE 1/3 mice in which one allele of ACE is null and the second allele was engineered to express ACE on the surface of hepatocytes. ACE 1/3 mice express no endothelial ACE and lack ACE within the lungs. Their kidneys contain <7.8% the enzyme levels present in control mice. Plasma conversion of angiotensin I to angiotensin II was 43.3% normal. The baseline blood pressure and renal function of the ACE 1/3 mice were normal, probably as a function of a marked increase of both plasma angiotensin I and angiotensin II. When exposed to 2 weeks of a salt-free diet (a stress diet stimulating the RAS), blood pressure in ACE 1/3 mice decreased to 92.3+/-2.0 mm Hg, a level significantly lower than that of wild-type control mice. The ACE 1/3 mice demonstrate the plasticity of the RAS and show that significant compensation is required to maintain normal, basal blood pressure in a mouse with an impaired local vascular and renal RAS.
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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/Angiotensin I,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Peptidyl-Dipeptidase A,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
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 |
1524-4563
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| pubmed:author | |
| pubmed:issnType |
Electronic
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| pubmed:volume |
41
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
313-21
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:12574101-Angiotensin I,
pubmed-meshheading:12574101-Angiotensin II,
pubmed-meshheading:12574101-Animals,
pubmed-meshheading:12574101-Blood Pressure,
pubmed-meshheading:12574101-Blotting, Western,
pubmed-meshheading:12574101-Endothelium, Vascular,
pubmed-meshheading:12574101-Female,
pubmed-meshheading:12574101-Genotype,
pubmed-meshheading:12574101-Heterozygote,
pubmed-meshheading:12574101-Kidney,
pubmed-meshheading:12574101-Liver,
pubmed-meshheading:12574101-Lung,
pubmed-meshheading:12574101-Male,
pubmed-meshheading:12574101-Mice,
pubmed-meshheading:12574101-Mice, Inbred C57BL,
pubmed-meshheading:12574101-Mice, Inbred Strains,
pubmed-meshheading:12574101-Mice, Knockout,
pubmed-meshheading:12574101-Peptidyl-Dipeptidase A,
pubmed-meshheading:12574101-Plasma Volume,
pubmed-meshheading:12574101-Sodium,
pubmed-meshheading:12574101-Sodium, Dietary
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| pubmed:year |
2003
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| pubmed:articleTitle |
Mice lacking endothelial ACE: normal blood pressure with elevated angiotensin II.
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| pubmed:affiliation |
Department of Pathology, Emory University, Atlanta, GA 30322, 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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