Mechanisms associated to impaired activity of cardiac P-type ATPases in endothelial nitric oxide synthase knockout mice

Mechanisms associated to impaired activity of cardiac P-type ATPases in endothelial nitric oxide synthase knockout mice

Author Rezende, Daniele C. Google Scholar
Pocas, Elisa S. C. Google Scholar
Muzi-Filho, Humberto Google Scholar
Cunha, Valeria M. N. Google Scholar
Caricati-Neto, Afonso Autor UNIFESP Google Scholar
Jurkiewicz, Aron Autor UNIFESP Google Scholar
Noel, Francois Google Scholar
Quintas, Luis E. M. Google Scholar
Institution Universidade Federal do Rio de Janeiro (UFRJ)
Insitituto Fed Educ Ciencia & Tecnol Rio de Janei
Universidade Federal de São Paulo (UNIFESP)
Abstract The effect of long-lasting in vivo restriction of nitric oxide (NO) bioavailability on cardiac and renal P-type ATPases critical for intracellular ion homeostasis is controversial. Previous work has shown in eNOS knockout (eNOS(-/-)) mice hearts that Na+/K+- and Ca2+-ATPase activities were depressed but the underlying mechanisms are still unclear. the goal of this study was to characterize potential alterations responsible for impaired enzyme activity in eNOS(-/-) mice. Na+/K+-ATPase activity from crude preparations of adult male eNOS(-/-) mice hearts and kidneys was reduced compared with wild-type animals (32 %, p < 0.05 and 16 %, p < 0.0001, respectively). Immunoblot analysis showed that although the expression of the predominant (or exclusive, for the kidney) Na+/K+-ATPase alpha 1 isoform was not significantly changed, there was an important downregulation of the less abundant alpha 2 isoform in the heart (57 %, p < 0.0001). in addition, although cardiac Ca2+-ATPase activity was unaltered, the expression of sarco/endoplasmic reticulum Ca2+-ATPase 2 protein in eNOS(-/-) mice was very high (290 % compared with wild-type animals, p < 0.0001) without any significant change in phospholamban expression. Consistent with these findings, the content of cardiac and renal free sulfhydryl groups, essential for the catalytic function of such ATPases, was decreased (23 %, p < 0.01 and 35 %, p < 0.05, respectively). Altogether, the present results suggest that the absence of eNOS promotes a compartmentalized altered redox balance that affects the activity and expression of ion transport ATPases.
Keywords eNOS knockout mice
Oxidative stress
Nitric oxide
Language English
Sponsor Fundação de Amparo à Pesquisa do Estado do Rio de Janeiro (FAPERJ)
Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Date 2013-06-01
Published in Journal of Physiology and Biochemistry. Pamplona: Servicio Publicaciones Universidad Navarra, v. 69, n. 2, p. 207-214, 2013.
ISSN 1138-7548 (Sherpa/Romeo, impact factor)
Publisher Servicio Publicaciones Universidad Navarra
Extent 207-214
Access rights Closed access
Type Article
Web of Science ID WOS:000318510700005

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