rdf:type |
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lifeskim:mentions |
umls-concept:C0015272,
umls-concept:C0020538,
umls-concept:C0026336,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0205419,
umls-concept:C0277785,
umls-concept:C0857121,
umls-concept:C1335671,
umls-concept:C1366535,
umls-concept:C1554184
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pubmed:issue |
1
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pubmed:dateCreated |
2002-5-1
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pubmed:abstractText |
Essential hypertension is a prevalent complex polygenic disease and a major risk factor for cardiovascular disease, the leading cause of death in developed countries. Because of its complex and multifactorial nature, its genetic determinants still remain largely unknown. The Dahl salt-sensitive hypertensive rat model exhibits impaired sodium handling, which is hypothesized to play a key role in the pathophysiology of polygenic hypertension. Thus, genes associated with renal regulation of salt and water balance are a priori likely candidates for a causative role in hypertension pathogenesis. The functional properties and renal-specific expression of the recently characterized AngII/AVP receptor suggest a putative modulator role in tubular sodium and fluid reabsorption. Based on these observations, we investigated the potential involvement of the AngII/AVP receptor in salt-sensitive hypertension.
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pubmed:grant |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Arginine Vasopressin,
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP,
http://linkedlifedata.com/resource/pubmed/chemical/DNA, Complementary,
http://linkedlifedata.com/resource/pubmed/chemical/Genetic Markers,
http://linkedlifedata.com/resource/pubmed/chemical/Ligands,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Angiotensin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Vasopressin,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Chloride
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1076-1551
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
8
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
24-32
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pubmed:dateRevised |
2008-11-20
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pubmed:meshHeading |
pubmed-meshheading:11984003-Allosteric Regulation,
pubmed-meshheading:11984003-Amino Acid Sequence,
pubmed-meshheading:11984003-Amino Acid Substitution,
pubmed-meshheading:11984003-Angiotensin II,
pubmed-meshheading:11984003-Animals,
pubmed-meshheading:11984003-Arginine Vasopressin,
pubmed-meshheading:11984003-Blood Pressure,
pubmed-meshheading:11984003-Chromosome Mapping,
pubmed-meshheading:11984003-Crosses, Genetic,
pubmed-meshheading:11984003-Cyclic AMP,
pubmed-meshheading:11984003-DNA, Complementary,
pubmed-meshheading:11984003-Genes,
pubmed-meshheading:11984003-Genetic Markers,
pubmed-meshheading:11984003-Genetic Predisposition to Disease,
pubmed-meshheading:11984003-Hypertension,
pubmed-meshheading:11984003-Kidney,
pubmed-meshheading:11984003-Ligands,
pubmed-meshheading:11984003-Lod Score,
pubmed-meshheading:11984003-Male,
pubmed-meshheading:11984003-Molecular Sequence Data,
pubmed-meshheading:11984003-Quantitative Trait, Heritable,
pubmed-meshheading:11984003-Rats,
pubmed-meshheading:11984003-Rats, Inbred Dahl,
pubmed-meshheading:11984003-Receptors, Angiotensin,
pubmed-meshheading:11984003-Receptors, Vasopressin,
pubmed-meshheading:11984003-Second Messenger Systems,
pubmed-meshheading:11984003-Sequence Homology,
pubmed-meshheading:11984003-Sodium,
pubmed-meshheading:11984003-Sodium Chloride
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pubmed:year |
2002
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pubmed:articleTitle |
The dual AngII/AVP receptor gene N119S/C163R variant exhibits sodium-induced dysfunction and cosegregates with salt-sensitive hypertension in the Dahl salt-sensitive hypertensive rat model.
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pubmed:affiliation |
Whitaker Cardiovascular Clinic, Boston, MA 02118, USA. nruizo@bu.edu
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.
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