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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6 Pt 2
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pubmed:dateCreated |
1998-11-5
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pubmed:abstractText |
To elucidate the contribution of the renin-angiontensin system (RAS) to glomerular injury in salt-sensitive hypertension, we investigated the chronic effects of the angiotensin I-converting enzyme inhibitor cilazapril and the angiotensin II type 1-receptor antagonist (AT1a) TCV-116 in Dahl-Iwai rats. Dahl salt-sensitive (S) rats receiving 8% salt diet for 6 wk were simultaneously treated with cilazapril (n = 6), TCV-116 (n = 6), or saline (n = 14). The 8% salt diet markedly increased systolic blood pressure (SBP), urinary protein, and N-acetyl-beta-glucosaminidase (NAG) excretion compared with 0.3% salt-treated S (n = 6) or salt-resistant (n = 6) rats. Although neither cilazapril nor TCV-116 reduced the elevated SBP, TCV-116 significantly lowered urinary protein and NAG excretion. Histologically, 8% salt treatment in S rats induced progressive sclerotic and proliferative glomerular changes, which were ameliorated by both drugs. TCV-116 increased the glomerular diameter. Immunofluorescence demonstrated the increased level of type III collagen in the mesangium of 8% salt-treated S rats, which was completely reversed by TCV-116. Competitive RT-PCR of mRNA extracted from the glomeruli revealed that 8% salt treatment significantly increased the levels of proliferating cell nuclear antigen (PCNA) and platelet-derived growth factor B-chain and that TCV-116 significantly reduced the levels of PCNA and transforming growth factor-beta1 (TGF-beta1). Thus, although the chronic RAS-inhibition in salt-sensitive hypertension exerted a histologically renoprotective effect by both ways without lowering blood pressure, the RAS inhibition due to AT1a had more beneficial advantages of reducing proteinuria and attenuating the levels of glomerular TGF-beta1 and extracellular matrix.
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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/Acetylglucosaminidase,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin Receptor Antagonists,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin-Converting Enzyme...,
http://linkedlifedata.com/resource/pubmed/chemical/Benzimidazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Biphenyl Compounds,
http://linkedlifedata.com/resource/pubmed/chemical/Cilazapril,
http://linkedlifedata.com/resource/pubmed/chemical/Creatinine,
http://linkedlifedata.com/resource/pubmed/chemical/Platelet-Derived Growth Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Proliferating Cell Nuclear Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Tetrazoles,
http://linkedlifedata.com/resource/pubmed/chemical/Transforming Growth Factor beta,
http://linkedlifedata.com/resource/pubmed/chemical/candesartan cilexetil
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0002-9513
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
274
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
R1797-806
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:9841488-Acetylglucosaminidase,
pubmed-meshheading:9841488-Angiotensin Receptor Antagonists,
pubmed-meshheading:9841488-Angiotensin-Converting Enzyme Inhibitors,
pubmed-meshheading:9841488-Animals,
pubmed-meshheading:9841488-Benzimidazoles,
pubmed-meshheading:9841488-Biphenyl Compounds,
pubmed-meshheading:9841488-Blood Pressure,
pubmed-meshheading:9841488-Body Weight,
pubmed-meshheading:9841488-Cilazapril,
pubmed-meshheading:9841488-Creatinine,
pubmed-meshheading:9841488-Heart Rate,
pubmed-meshheading:9841488-Kidney Glomerulus,
pubmed-meshheading:9841488-Platelet-Derived Growth Factor,
pubmed-meshheading:9841488-Proliferating Cell Nuclear Antigen,
pubmed-meshheading:9841488-Proteinuria,
pubmed-meshheading:9841488-Rats,
pubmed-meshheading:9841488-Rats, Inbred Dahl,
pubmed-meshheading:9841488-Sclerosis,
pubmed-meshheading:9841488-Tetrazoles,
pubmed-meshheading:9841488-Transforming Growth Factor beta,
pubmed-meshheading:9841488-Urine
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pubmed:year |
1998
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pubmed:articleTitle |
Effects of chronic inhibition of ACE and AT1 receptors on glomerular injury in dahl salt-sensitive rats.
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pubmed:affiliation |
Department of Medicine III, Okayama University Medical School, Okayama University, Okayama 700-8558 Japan.
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pubmed:publicationType |
Journal Article
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