Autor(es)

C.M. Pertrini ^[1] ; A.A. Miyakawa ^[2] ; F.R.M. Laurindo ^[3] ; J.E. Krieger ^[4]

Afiliação do(s) autor(es)

^[1] Universidade de São Paulo. Faculdade de Medicina. Instituto do Coração (InCor)

^[2] Universidade de São Paulo. Faculdade de Medicina. Instituto do Coração (InCor)

^[3] Universidade de São Paulo. Faculdade de Medicina. Instituto do Coração (InCor) - Brasil

^[4] Universidade de São Paulo. Faculdade de Medicina. Instituto do Coração (InCor)

• Tipo de documento: Artigo Científico
• Fonte: Brazilian Journal of Medical and Biological Research; v. 36, n. 9, p. 1175-1178, 2003-09-00.

Resumo

Mechanical forces including pressure and shear stress play an important role in vascular homeostasis via the control of the production and release of a variety of vasoactive factors. An increase in vascular shear stress is accompanied by nitric oxide (NO) release and NO synthase activation. Previously, we have demonstrated that shear stress induces angiotensin-I converting enzyme (ACE) down-regulation in vivo and in vitro. In the present study, we determined whether NO participates in the shear stress-induced ACE suppression response. Rabbit aortic endothelial cells were evaluated using the NO synthase inhibitor L-NAME, and two NO donors, diethylamine NONOate (DEA/NO) and sodium nitroprusside (SNP). Under static conditions, incubation of endothelial cells with 1 mM L-NAME for 18 h increased ACE activity by 27% (from 1.000 ± 0.090 to 1.272 ± 0.182) while DEA/NO and SNP (0.1, 0.5 and 1 mM) caused no change in ACE activity. Interestingly, ACE activity was down-regulated similarly in the presence or absence of L-NAME (delta(0 mM) = 0.26 ± 0.055, delta(0.1 mM) = 0.21 ± 0.22, delta(1 mM) = 0.36 ± 0.13) upon 18 h shear stress activation (from static to 15 dyn/cm²). Taken together, these results indicate that NO can participate in the maintenance of basal ACE levels in the static condition but NO is not associated with the shear stress-induced inactivation of ACE. (AU)

• Processo FAPESP: 01/00009-0 - Estudo integrado da hipertensão arterial: caracterização molecular e funcional do sistema cardiovascular
• Beneficiário: Eduardo Moacyr Krieger
• Modalidade de apoio: Auxílio à Pesquisa - Temático
• Processo FAPESP: 00/09485-7 - Identificacao de genes com expressao diferenciada em veia safena submetida ao regime arterial.
• Beneficiário: Ayumi Aurea Miyakawa Yamaguchi
• Modalidade de apoio: Bolsas no Brasil - Pós-Doutorado
• Processo FAPESP: 00/06639-3 - Participacao do oxido nitrico na reducao da enzima conversora de angiotensina i induzida pelo "shear stress".
• Beneficiário: Carla Moniz Pertrini
• Modalidade de apoio: Bolsas no Brasil - Iniciação Científica
• Processo FAPESP: 00/12154-2 - Fisiologia molecular da sinalização redox no sistema vascular e modelos de células em cultura
• Beneficiário: Francisco Rafael Martins Laurindo
• Modalidade de apoio: Auxílio à Pesquisa - Temático