dc.creatorLehfeld, LS
dc.creatorSilveira, LA
dc.creatorGhini, B
dc.creatorde Faria, JBL
dc.date2004
dc.date2014-08-01T18:29:48Z
dc.date2015-11-26T18:05:01Z
dc.date2014-08-01T18:29:48Z
dc.date2015-11-26T18:05:01Z
dc.date.accessioned2018-03-29T00:47:15Z
dc.date.available2018-03-29T00:47:15Z
dc.identifierKidney & Blood Pressure Research. Karger, v. 27, n. 2, n. 114, n. 120, 2004.
dc.identifier1420-4096
dc.identifierWOS:000221112800007
dc.identifier10.1159/000077535
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/79719
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/79719
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1293015
dc.descriptionBackground/Aims: This study tested the hypothesis that prevention of the development of hypertension, and not the class of antihypertensive agent, inhibits the increase in renal fibronectin and albuminuria in experimental diabetes. Methods: Four-week-old spontaneously hypertensive rats (SHR), with diabetes induced by streptozotocin, were randomized for no treatment, or treatment with captopril, amlodipine, an association of captopril and amlodipine (Cap+A) or an association of captopril and verapamil (Cap+V) for 12 weeks. Results: Systolic blood pressure increased similarly in control (187 +/- 5 mm Hg, mean +/- SE) and diabetic (186 +/- 4) SHR and was kept within the normal range by amlodipine (131 +/- 3), captopril (127 +/- 3), Cap+A (134 +/- 4) and Cap+V (134 +/- 9, p < 0.0001). In diabetic rats, albuminuria was higher than in control SHR [geometric mean (variance), 1,213 ( 953 1,708) vs. 512 (213-850), p < 0.0001] and was reduced to a similar extent by amlodipine [573 (353-744), p < 0.0001], captopril [562 (238-771), p < 0.0001], Cap+A [679 (442-971), p < 0.0001] and Cap+V [748 (581-848) &mu;g/24 h, p = 0.0002]. Renal fibronectin increased in diabetic rats (24.0 &PLUSMN; 3.3 densitometric units, mean &PLUSMN; SE) compared to control rats (9.6 &PLUSMN; 1.8, p = 0.0005) and was normalized by amlodipine (9.9 &PLUSMN; 1.0, p = 0.0001), captopril (11.2 &PLUSMN; 0.4, p = 0.0016), Cap+A (9.9 &PLUSMN; 2.0, p = 0.0004) and Cap+V (14.7 &PLUSMN; 4.9, p = 0.0159). Conclusion: In this model, tight blood pressure control rather than the class of antihypertensive agent was the main determinant factor in attenuating of nephropathy. Copyright (C) 2004 S. Karger AG, Basel.
dc.description27
dc.description2
dc.description114
dc.description120
dc.languageen
dc.publisherKarger
dc.publisherBasel
dc.publisherSuíça
dc.relationKidney & Blood Pressure Research
dc.relationKidney Blood Pressure Res.
dc.rightsaberto
dc.rightshttp://www.karger.com/Services/RightsPermissions
dc.sourceWeb of Science
dc.subjecthypertension
dc.subjectdiabetes mellitus
dc.subjectdiabetic nephropathy
dc.subjectspontaneously hypertensive rats
dc.subjectrenin-angiotensin system
dc.subjectfibronectin
dc.subjectConverting Enzyme-inhibition
dc.subjectGenetic-hypertension
dc.subjectProteinuria
dc.subjectProgression
dc.subjectTherapy
dc.subjectRat
dc.subjectInsufficiency
dc.subjectComplications
dc.subjectRisk
dc.titleEarly blood pressure normalization independent of the class of antihypertensive agent prevents augmented renal fibronectin and albuminuria in experimental diabetic nephropathy
dc.typeArtículos de revistas


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