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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.)


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Fernandes, Tiago [1] ; Magalhaes, Flavio de Castro [1, 2, 3] ; do Carmo, Everton Crivoi [1] ; de Oliveira, Edilamar Menezes [1]
Total Authors: 4
[1] Univ Sao Paulo, Phys Educ & Sports Sch, Lab Biochem & Mol Biol Exercise, BR-05508900 Sao Paulo - Brazil
[2] Fed Univ Jequitinhonha, Exercise Biol Lab, Biol & Hlth Sci Sch, Diamantina, MG - Brazil
[3] Fed Univ Mucuri Valleys, Diamantina, MG - Brazil
Total Affiliations: 3
Document type: Journal article
Source: Revista Brasileira de Medicina do Esporte; v. 18, n. 6, p. 412-418, NOV-DEC 2012.
Web of Science Citations: 0

Aerobic exercise training (ET) has been established as an important non-pharmacological treatment for hypertension, since it corrects the microvascular rarefaction and decreases blood pressure. Studies have shown that microvascular abnormalities are directly associated with changes in the vascular endothelial growth factor (VEGF) and VEGF receptor 2 (VEGFR2), as well as with imbalance of apoptotic signaling in hypertension. However, little is known about these mechanisms in hypertension. We hypothesized that ET restores angiogenic factors and promotes balance between anti and pro-apoptotic proteins of the Bcl-2 family, potentially contributing to revascularization and the disease regression. Twelve-week old male Spontaneously Hypertensive Rats (SHR, n=14) and Wistar Kyoto Rats (WKY, n=14) were randomly assigned into 4 groups: SHR, trained SHR (SHR-T), WKY and trained WKY (WKY-T) were studied. As expected, ten weeks of ET were effective in reducing blood pressure in SHR-T group. In addition, ET promoted resting bradycardia in trained groups (WKY-T and SHR-T), being considered an important marker of aerobic ET. ET has also corrected the capillary rarefaction in SHR-T and this response is partly due to recovery of the peripheral levels of VEGF and increase in VEGFR2 expression. Concomitantly, normalization of the apoptotic pathway was observed, with increased expression of the anti-apoptotic proteins (Bcl-2 and Bcl-x) and reduction of the pro-apoptotic protein (Bad), followed by phosphorylation of the Bad protein and decrease in the Bad/Bcl-x association. These data suggest that ET promotes peripheral revascularization in hypertension dependent on a fine balance between positive and negative regulators of angiogenesis. (AU)

FAPESP's process: 10/50048-1 - Cellular and functional bases of exercise in cardiovascular diseases
Grantee:Carlos Eduardo Negrão
Support type: Research Projects - Thematic Grants