| Full text | |
| Author(s): |
Total Authors: 4
|
| Affiliation: | [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)
Total Affiliations: 4
|
| Document type: | Journal article |
| Source: | Brazilian Journal of Medical and Biological Research; v. 36, n. 9, p. 1175-1178, 2003-09-00. |
| Abstract | |
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) | |
| FAPESP's process: | 01/00009-0 - An integrated approach for the dissection of primary hypertension: molecular and functional characterization of the cardiovascular system |
| Grantee: | Eduardo Moacyr Krieger |
| Support Opportunities: | Research Projects - Thematic Grants |
| FAPESP's process: | 00/12154-2 - Molecular physiology of redox signaling in the vascular system and cultured cell models |
| Grantee: | Francisco Rafael Martins Laurindo |
| Support Opportunities: | Research Projects - Thematic Grants |