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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Overexpression of Urinary N-Domain ACE in Chronic Kidney Dysfunction in Wistar Rats

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Author(s):
Arita, Danielle Yuri [1] ; Cunha, Tatiana Sousa [2, 1] ; Perez, Juliana Dineia [1] ; Colucci, Juliana Almada [1, 3] ; Ronchi, Fernanda Aparecida [1] ; Nogueira, Marie Doki [1] ; Arita, Lilian Saemi [1] ; Aragao, Danielle Sanches [1] ; Castro Teixeira, Vicente de Paulo [1] ; Casarini, Dulce Elena [1]
Total Authors: 10
Affiliation:
[1] Univ Fed Sao Paulo, Sch Med, Dept Med, Div Nephrol, Sao Paulo - Brazil
[2] Univ Fed Sao Paulo, Inst Sci & Technol, Sao Paulo - Brazil
[3] Cleveland Clin, Lerner Res Inst, Cleveland, OH 44106 - USA
Total Affiliations: 3
Document type: Journal article
Source: CLINICAL AND EXPERIMENTAL HYPERTENSION; v. 34, n. 6, p. 389-396, 2012.
Web of Science Citations: 3
Abstract

Local activation of the renin-angiotensin system (RAS) has been implicated in the pathogenesis of several renal disorders. In this study we investigated how chronic kidney disease (CKD) modulates RAS components in an experimental model. Male Wistar rats were divided into three groups: sham, nephrectomized, and nephrectomized receiving losartan. Chronic kidney disease animals presented decreased renal N-domain angiotensin-converting enzyme (ACE) activity but overexpression of N-domain ACE in urine. Remnant kidneys presented high angiotensin II levels. Losartan treatment increased urine and tissue ACE activity and tissue levels of angiotensins, mainly angiotensin (1-7), and improved renal and histopathologic parameters. Taken together, the authors' results indicate that pathophysiological changes due to CKD could lead to an increased expression of somatic and N-domain ACE, mainly the 65 kDa isoform, suggesting that this enzyme could be used as a biological urinary marker in CKD. (AU)

FAPESP's process: 02/13290-2 - Angiotensin I: converting enzyme isoform (90 kDa), potential genetic marker of hypertension: processing, molecular and functional characterization, and genetic segregation
Grantee:Dulce Elena Casarini
Support Opportunities: Research Projects - Thematic Grants