Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/34512
Title: Overexpression of Urinary N-Domain ACE in Chronic Kidney Dysfunction in Wistar Rats
Authors: Arita, Danielle Yuri [UNIFESP]
Cunha, Tatiana Sousa [UNIFESP]
Perez, Juliana Dineia [UNIFESP]
Colucci, Juliana Almada [UNIFESP]
Ronchi, Fernanda Aparecida [UNIFESP]
Nogueira, Marie Doki [UNIFESP]
Arita, Lilian Saemi [UNIFESP]
Aragao, Danielle Sanches [UNIFESP]
Teixeira, Vicente de Paulo Castro [UNIFESP]
Casarini, Dulce Elena [UNIFESP]
Universidade Federal de São Paulo (UNIFESP)
Cleveland Clin
Keywords: angiotensin-converting enzyme
angiotensins
hypertension
chronic kidney disease
Issue Date: 1-Jan-2012
Publisher: Informa Healthcare
Citation: Clinical and Experimental Hypertension. London: Informa Healthcare, v. 34, n. 6, p. 389-396, 2012.
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.
URI: http://repositorio.unifesp.br/handle/11600/34512
ISSN: 1064-1963
Other Identifiers: http://dx.doi.org/10.3109/10641963.2011.649932
Appears in Collections:Em verificação - Geral

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