Linked Life Data

9016898

Source:http://linkedlifedata.com/resource/pubmed/id/9016898

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1997-2-26
pubmed:abstractText
In several models of renal disease progression, angiotensin-converting enzyme (ACE) inhibitors reduced proteinuria and limited glomerulosclerosis, which suggested that reduction of renal angiotensin II (Ang II) activity is crucial for the preservation of glomerular structure and function. However, it cannot be ruled out that other hormonal systems, including inhibition of the bradykinin breakdown, also play a role. We compared the effects of chronic treatment with the ACE inhibitor lisinopril with those of a specific Ang II receptor antagonist, L-158,809, on proteinuria and renal injury in passive Heymann nephritis (PHN), a model of immune renal disease that closely resembles human membranous nephropathy, with long-lasting proteinuria followed by tubulointerstitial damage and glomerulosclerosis. Passive Heymann nephritis was induced with 0.5 mL/100 g of rabbit anti-Fx1A antibody in 24 male Sprague-Dawley rats. The animals were divided into three groups of eight rats each, and were given the following in the drinking water on a daily basis: lisinopril (40 mg/L), L-158,809 (50 mg/L), or no therapy. Treatment started at day 7 (proteinuria was already present) and lasted 12 months. Eight normal rats were used as controls. Untreated PHN rats developed hypertension, while rats with PHN given lisinopril or L-158,809 all had systolic blood pressure values even lower than those of normal rats. Urinary protein excretion progressively increased with time in untreated PHN rats, who developed tubulointerstitial damage and glomerulosclerosis. Both lisinopril and L-158,809 exhibited a potent antiproteinuric effect and preserved glomerular and tubular structural integrity at a similar extent. Renal gene expression of transforming growth factor-beta and extracellular matrix proteins was also effectively reduced by the two treatments. These results indicate that ACE inhibitors and Ang II receptor antagonists are equally effective in preventing renal injury in PHN and suggest that the renoprotective effects of ACE inhibitors in this model are solely due to inhibition of Ang II.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0272-6386
pubmed:author
pubmed:issnType
Print
pubmed:volume
29
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
254-64
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:9016898-Angiotensin II, pubmed-meshheading:9016898-Angiotensin Receptor Antagonists, pubmed-meshheading:9016898-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:9016898-Animals, pubmed-meshheading:9016898-Blood Pressure, pubmed-meshheading:9016898-Chronic Disease, pubmed-meshheading:9016898-Extracellular Matrix Proteins, pubmed-meshheading:9016898-Glomerular Filtration Rate, pubmed-meshheading:9016898-Glomerulonephritis, Membranous, pubmed-meshheading:9016898-Imidazoles, pubmed-meshheading:9016898-Kidney, pubmed-meshheading:9016898-Lisinopril, pubmed-meshheading:9016898-Male, pubmed-meshheading:9016898-Proteinuria, pubmed-meshheading:9016898-Rats, pubmed-meshheading:9016898-Rats, Sprague-Dawley, pubmed-meshheading:9016898-Renal Plasma Flow, pubmed-meshheading:9016898-Tetrazoles, pubmed-meshheading:9016898-Transforming Growth Factor beta
pubmed:year
1997
pubmed:articleTitle
The renoprotective properties of angiotensin-converting enzyme inhibitors in a chronic model of membranous nephropathy are solely due to the inhibition of angiotensin II: evidence based on comparative studies with a receptor antagonist.
pubmed:affiliation
Mario Negri Institute for Pharmacological Research, Bergamo, Italy.
pubmed:publicationType
Journal Article, Comparative Study