Linked Life Data

11269510

Source:http://linkedlifedata.com/resource/pubmed/id/11269510

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2001-3-27
pubmed:abstractText
The renal endothelin (ET) system, particularly the ET type B receptor, has been implicated in the regulation of sodium excretion and glomerular filtration rate (GFR). We analyzed kidney morphology and function in a rat strain characterized by complete absence of a functional ETB receptor. Due to Hirschsprung's disease limiting lifetime in these rats, studies were performed in 23-day-old rats. Kidney size and morphology (glomerular and interstitial matrix content, glomerular size and cell density and intrarenal vascular morphology) were normal in ETB-deficient rats. There were also no evidence of altered kidney cell cycle regulation in these rats. GFR was significantly lower, by 72% (P<0.001), in homozygous ETB-deficient rats than in wild-type rats. Fractional sodium excretion was likewise markedly reduced by 84% in homozygous ETB-deficient rats (P<0.001 versus wild-type rats). Treatment with the specific epithelial sodium channel blocker amiloride led to a much higher increase in fractional sodium excretion in ETB-deficient rats (934.2+/-73% in ETB-deficient rats versus 297+/-20% in wild-type rats, expressed as percentage of corresponding placebo treated control; P<0.001). Mean arterial blood pressure was elevated by 7.9 mmHg in homozygous ETB-deficient rats (P<0.05 versus wild-type rats). Our study demonstrates that ETB-deficiency causes early onset kidney dysfunction characterized by a markedly reduced sodium excretion, decreased GFR, and slightly elevated blood pressure. The complete absence of the ETB receptor causes in the kidney--in contrast to the colon--a functional rather than a developmental, neural crest cell dependent disease, since kidney morphology was normal in ETB-deficient rats. The much higher increase in the fractional sodium excretion in ETB-deficient rats after pharmacological blockade of the epithelial sodium channel indicates that the decreased fractional sodium excretion in ETB-deficient rats is most probably due to a lack of the inhibitory property of the ETB receptor on the epithelial sodium channel activity.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0946-2716
pubmed:author
pubmed:issnType
Print
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
633-41
pubmed:dateRevised
2011-7-8
pubmed:meshHeading
pubmed-meshheading:11269510-Amiloride, pubmed-meshheading:11269510-Animals, pubmed-meshheading:11269510-Apoptosis, pubmed-meshheading:11269510-Arteries, pubmed-meshheading:11269510-Blood Pressure, pubmed-meshheading:11269510-Bromodeoxyuridine, pubmed-meshheading:11269510-Creatinine, pubmed-meshheading:11269510-Genotype, pubmed-meshheading:11269510-Glomerular Filtration Rate, pubmed-meshheading:11269510-Homozygote, pubmed-meshheading:11269510-Hypertension, pubmed-meshheading:11269510-In Situ Nick-End Labeling, pubmed-meshheading:11269510-Kidney, pubmed-meshheading:11269510-Organ Size, pubmed-meshheading:11269510-Polymerase Chain Reaction, pubmed-meshheading:11269510-Rats, pubmed-meshheading:11269510-Receptor, Endothelin B, pubmed-meshheading:11269510-Receptors, Endothelin, pubmed-meshheading:11269510-Sodium, pubmed-meshheading:11269510-Sodium Channel Blockers
pubmed:year
2001
pubmed:articleTitle
Impaired sodium excretion, decreased glomerular filtration rate and elevated blood pressure in endothelin receptor type B deficient rats.
pubmed:affiliation
Department of Nephrology, University Hospital Charité, Humboldt University of Berlin, Germany. berthold.hocher@rz.hu-berlin.de
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't