Linked Life Data

9375831

Source:http://linkedlifedata.com/resource/pubmed/id/9375831

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1997-12-16
pubmed:abstractText
Two substrains of the fawn-hooded (FH) rat have been developed, one of which develops progressive hypertension and proteinuria, the FHH, and one which shows little increase in blood pressure and no renal damage, the FHL. Other hypertensive rodent models show primary metabolic disturbances before the development of renal damage, notably hypertriglyceridemia, which may also contribute to progression of renal disease. In this study we evaluated whether hyperlipidemia is a primary disturbance in FHH, or only occurs secondary to proteinuria. Lipid levels were determined before and after development of proteinuria, and compared to those found in age-matched FHL. We also determined whether reducing proteinuria with lisinopril would normalize lipid levels in aging FHH. At 4 weeks of age, proteinuria was very low (2-3 mg/day) in both FHH and FHL. While proteinuria increased steadily in aging FHH, reaching 350 +/- 62 mg/day at 40 weeks, much less increase was observed in FHL over the same period (32 +/- 5 mg/day at 40 weeks). Blood pressure was markedly higher in adult FHH than in FHL (158 +/- 2 vs. 129 +/- 2 mm Hg, p < 0.01). In 4-week-old FHL and FHH, plasma cholesterol levels were similar. Subsequently, cholesterol increased in FHH, reaching 3.4 +/- 0.9 mmol/l at 40 weeks, whereas cholesterol was barely affected by aging in FHL (2.1 +/- 0.2 mmol/l at 40 weeks). At 4 weeks, triglyceride levels were lowest in FHH. Subsequently, triglycerides increased in FHH, reaching 3.5 +/- 1.5 mmol/l at 40 weeks, as compared to 1.3 +/- 0.2 mmol/l in FHL. Besides a transient increase in triglyerides in lisinopril-treated FHH at 11 weeks, increments in blood pressure, proteinuria, cholesterol, triglycerides and apolipoproteins A-I, B and E aging FHH were effectively prevented by lisinopril. These data strongly suggest that there is no primary difference in lipid metabolism between FHH and FHL and that changes in plasma lipids in FHH as compared to FHL are all secondary to proteinuria.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0028-2766
pubmed:author
pubmed:issnType
Print
pubmed:volume
77
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
346-52
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:9375831-Angiotensin-Converting Enzyme Inhibitors, pubmed-meshheading:9375831-Animals, pubmed-meshheading:9375831-Antihypertensive Agents, pubmed-meshheading:9375831-Apolipoproteins, pubmed-meshheading:9375831-Blood Pressure, pubmed-meshheading:9375831-Body Weight, pubmed-meshheading:9375831-Cholesterol, pubmed-meshheading:9375831-Creatinine, pubmed-meshheading:9375831-Disease Models, Animal, pubmed-meshheading:9375831-Hyperlipidemias, pubmed-meshheading:9375831-Hypertension, pubmed-meshheading:9375831-Lisinopril, pubmed-meshheading:9375831-Male, pubmed-meshheading:9375831-Osmotic Pressure, pubmed-meshheading:9375831-Proteinuria, pubmed-meshheading:9375831-Rats, pubmed-meshheading:9375831-Rats, Inbred Strains, pubmed-meshheading:9375831-Statistics as Topic, pubmed-meshheading:9375831-Triglycerides
pubmed:year
1997
pubmed:articleTitle
Hyperlipidemia is secondary to proteinuria and is completely normalized by angiotensin-converting enzyme inhibition in hypertensive fawn-hooded rats.
pubmed:affiliation
Department of Pediatric Surgery, Erasmus University Rotterdam, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't