Source:http://linkedlifedata.com/resource/pubmed/id/11459925
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
2001-7-18
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pubmed:abstractText |
A genetic variant of the gene for the alpha(1)-isoform of Na(+)-K(+)-ATPase (Atp1a1) was suggested to be involved in the pathogenesis of salt hypertension in Dahl rats through altered Na(+):K(+) coupling ratio. We studied Na(+)-K(+) pump activity in erythrocytes of Dahl salt-sensitive (SS/Jr) rats in relation to plasma lipids and blood pressure (BP) and the linkage of polymorphic microsatellite marker D2Arb18 (located within intron 1 and exon 2 of Atp1a1 gene) with various phenotypes in 130 SS/Jr x SR/Jr F(2) rats. Salt-hypertensive SS/Jr rats had higher erythrocyte Na(+) content, enhanced ouabain-sensitive (OS) Na(+) and Rb(+) transport, and higher Na(+):Rb(+) coupling ratio of the Na(+)-K(+) pump. BP of F(2) hybrids correlated with erythrocyte Na(+) content, OS Na(+) extrusion, and OS Na(+):Rb(+) coupling ratio, but not with OS Rb(+) uptake. In F(2) hybrids there was a significant association indicating suggestive linkage (P < 0.005, LOD score 2.5) of an intragenic marker D2Arb18 with pulse pressure but not with mean arterial pressure or any parameter of Na(+)-K(+) pump activity (including its Na(+):Rb(+) coupling ratio). In contrast, plasma cholesterol, which was elevated in salt-hypertensive Dahl rats and which correlated with BP in F(2) hybrids, was also positively associated with OS Na(+) extrusion. The abnormal Na(+):K(+) stoichiometry of the Na(+)-K(+) pump is a consequence of elevated erythrocyte Na(+) content and suppressed OS Rb(+):K(+) exchange. In conclusion, abnormal cholesterol metabolism but not the Atp1a1 gene locus might represent an important factor for both high BP and altered Na(+)-K(+) pump function in salt-hypertensive Dahl rats.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cholesterol,
http://linkedlifedata.com/resource/pubmed/chemical/Enzyme Inhibitors,
http://linkedlifedata.com/resource/pubmed/chemical/Lipids,
http://linkedlifedata.com/resource/pubmed/chemical/Ouabain,
http://linkedlifedata.com/resource/pubmed/chemical/Rubidium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium Chloride,
http://linkedlifedata.com/resource/pubmed/chemical/Sodium-Potassium-Exchanging ATPase
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pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
1531-2267
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
17
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pubmed:volume |
6
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
99-104
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11459925-Animals,
pubmed-meshheading:11459925-Blood Pressure,
pubmed-meshheading:11459925-Cholesterol,
pubmed-meshheading:11459925-Enzyme Inhibitors,
pubmed-meshheading:11459925-Erythrocytes,
pubmed-meshheading:11459925-Hypertension,
pubmed-meshheading:11459925-Ion Transport,
pubmed-meshheading:11459925-Lipids,
pubmed-meshheading:11459925-Male,
pubmed-meshheading:11459925-Ouabain,
pubmed-meshheading:11459925-Polymorphism, Genetic,
pubmed-meshheading:11459925-Rats,
pubmed-meshheading:11459925-Rats, Inbred Dahl,
pubmed-meshheading:11459925-Rubidium,
pubmed-meshheading:11459925-Sodium,
pubmed-meshheading:11459925-Sodium Chloride,
pubmed-meshheading:11459925-Sodium-Potassium-Exchanging ATPase
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pubmed:year |
2001
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pubmed:articleTitle |
Altered Na+-K+ pump activity and plasma lipids in salt-hypertensive Dahl rats: relationship to Atp1a1 gene.
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pubmed:affiliation |
Institute of Physiology, Academy of Sciences of the Czech Republic, Center for Experimental Research of Cardiovascular Diseases, CZ-142 20 Prague, Czech Republic. zicha@biomed.cas.cz
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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