pubmed-article:20404220 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20404220 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
pubmed-article:20404220 | lifeskim:mentions | umls-concept:C0022646 | lld:lifeskim |
pubmed-article:20404220 | lifeskim:mentions | umls-concept:C0013030 | lld:lifeskim |
pubmed-article:20404220 | lifeskim:mentions | umls-concept:C0037473 | lld:lifeskim |
pubmed-article:20404220 | lifeskim:mentions | umls-concept:C0596902 | lld:lifeskim |
pubmed-article:20404220 | lifeskim:mentions | umls-concept:C0041904 | lld:lifeskim |
pubmed-article:20404220 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:20404220 | pubmed:dateCreated | 2010-5-20 | lld:pubmed |
pubmed-article:20404220 | pubmed:abstractText | D(5) dopamine receptor (D(5)R)-deficient (D(5)(-/-)) mice have hypertension that is aggravated by an increase in sodium intake. The present experiments were designed to test the hypothesis that a dysregulation of renal sodium transporters is related to the salt sensitivity in D(5)(-/-) mice. D(5)R was expressed in the renal proximal tubule, thick ascending limb, distal convoluted tubule, and cortical and outer medullary collecting ducts in D(5)(+/+) mice. On a control Na(+) diet, renal protein expressions of NKCC2 (sodium-potassium-2 chloride cotransporter), sodium chloride cotransporter, and alpha and gamma subunits of the epithelial sodium channel were greater in D(5)(-/-) than in D(5)(+/+) mice. Renal renin abundance and urine aldosterone levels were similar but renal angiotensin II type 1 receptor (AT(1)R) protein expression was increased in D(5)(-/-) mice. An elevated Na(+) diet increased further the elevated blood pressure of D(5)(-/-) mice but did not affect the normal blood pressure of D(5)(+/+) mice. The increased levels of NKCC2, sodium chloride cotransporter, and alpha and gamma subunits of the epithelial sodium channel persisted with the elevated Na(+) diet and unaffected by chronic AT(1)R blockade (losartan) in D(5)(-/-) mice. The expressions of proximal sodium transporters NHE3 (sodium hydrogen exchanger type 3) and NaPi2 (sodium phosphate cotransporter type 2) were increased by the elevated Na(+) diet in D(5)(-/-) mice; the increased expression of NHE3 but not NaPi2 was abolished by AT(1)R blockade. Our findings suggest that the increased protein expression of sodium transporters/channels in distal nephron segments may be the direct consequence of the disruption of D(5)R, independent of the renin-angiotensin aldosterone system. | lld:pubmed |
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pubmed-article:20404220 | pubmed:language | eng | lld:pubmed |
pubmed-article:20404220 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20404220 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20404220 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:20404220 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20404220 | pubmed:month | Jun | lld:pubmed |
pubmed-article:20404220 | pubmed:issn | 1524-4563 | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:JosePedro APA | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:EisnerGilbert... | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:WangXiaoyanX | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:ArmandoInesI | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:JonesJohn EJE | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:SibleyDavid... | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:YangZhiweiZ | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:LiHewangH | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:LuoYingjinY | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:AsicoLaureano... | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:EscanoCrisant... | lld:pubmed |
pubmed-article:20404220 | pubmed:author | pubmed-author:LuQuanshengQ | lld:pubmed |
pubmed-article:20404220 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20404220 | pubmed:volume | 55 | lld:pubmed |
pubmed-article:20404220 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20404220 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20404220 | pubmed:pagination | 1431-7 | lld:pubmed |
pubmed-article:20404220 | pubmed:dateRevised | 2011-9-26 | lld:pubmed |
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