| Texto completo | |
| Autor(es): |
Silva, Jr., Jose Antonio
[1, 2]
;
Santana, Eduardo Tadeu
[1]
;
Manchini, Martha Trindade
[1]
;
Antonio, Ednei Luis
[3]
;
Bocalini, Danilo Sales
[1]
;
Krieger, Jose Eduardo
[4]
;
Ferreira Tucci, Paulo Jose
[3]
;
Serra, Andrey Jorge
[1, 2]
Número total de Autores: 8
|
| Afiliação do(s) autor(es): | [1] Univ Nove Julho Uninove, Programa Posgrad Ciencias Reabilitacao, Sao Paulo - Brazil
[2] Univ Nove Julho Uninove, Programa Posgrad Med, Sao Paulo - Brazil
[3] Univ Fed Sao Paulo UNIFESP, Sao Paulo - Brazil
[4] Univ Sao Paulo, Sao Paulo - Brazil
Número total de Afiliações: 4
|
| Tipo de documento: | Artigo Científico |
| Fonte: | PLoS One; v. 9, n. 3 MAR 10 2014. |
| Citações Web of Science: | 8 |
| Resumo | |
Sympathetic hyperactivity induces adverse effects in myocardial. Recent studies have shown that exercise training induces cardioprotection against sympathetic overload; however, relevant mechanisms of this issue remain unclear. We analyzed whether exercise can prevent pathological hypertrophy induced by sympathetic hyperactivity with modulation of the kallikrein-kinin and angiogenesis pathways. Male Wistar rats were assigned to non-trained group that received vehicle; non-trained isoproterenol treated group (Iso, 0.3 mg kg(-1) day(-1)); and trained group (Iso+Exe) which was subjected to sympathetic hyperactivity with isoproterenol. The Iso rats showed hypertrophy and myocardial dysfunction with reduced force development and relaxation of muscle. The isoproterenol induced severe fibrosis, apoptosis and reduced myocardial capillary. Interestingly, exercise blunted hypertrophy, myocardial dysfunction, fibrosis, apoptosis and capillary decreases. The sympathetic hyperactivity was associated with high abundance of ANF mRNA and beta-MHC mRNA, which was significantly attenuated by exercise. The tissue kallikrein was augmented in the Iso+Exe group, and kinin B-1 receptor mRNA was increased in the Iso group. Moreover, exercise induced an increase of kinin B-2 receptor mRNA in myocardial. The myocardial content of eNOS, VEGF, VEGF receptor 2, pAkt and Bcl-2 were increased in the Iso+Exe group. Likewise, increased expression of pro-apoptotic Bad in the Iso rats was prevented by prior exercise. Our results represent the first demonstration that exercise can modulate kallikrein-kinin and angiogenesis pathways in the myocardial on sympathetic hyperactivity. These findings suggest that kallikrein-kinin and angiogenesis may have a key role in protecting the heart. (AU) | |
| Processo FAPESP: | 09/54225-8 - Fisiopatologia da insuficiência cardíaca congestiva |
| Beneficiário: | Paulo Jose Ferreira Tucci |
| Modalidade de apoio: | Auxílio à Pesquisa - Temático |