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Effect of different intensities of aerobic exercise training on cardiac function and hypertrophy of spontaneously hypertensive rats: role of ANG (1-7)

Grant number: 12/19896-1
Support type:Scholarships abroad - Research
Effective date (Start): March 15, 2013
Effective date (End): March 14, 2014
Field of knowledge:Health Sciences - Physical Education
Principal researcher:Alessandra Medeiros
Grantee:Alessandra Medeiros
Host: Ulrik Wisløff
Home Institution: Instituto de Saúde e Sociedade (ISS). Universidade Federal de São Paulo (UNIFESP). Campus Baixada Santista. Santos , SP, Brazil
Research place: Norwegian University of Science and Technology (NTNU), Norway  

Abstract

Despite scientific advances in the treatment of hypertension, the number of hypertensive individuals has increased each year. The hemodynamic stress due to pressure regimes too high can lead to heart disease, nephropathy, hypertensive retinopathy, and is also a major factor in the development of cardiac remodeling observed in hypertensive individuals. Important to remember that cardiac remodeling is directly related to progression of compensated cardiac hypertrophy observed in hypertensive individuals, for heart failure. Some intracellular signaling pathways have been implicated in pathological cardiac remodeling observed in hypertension. The via calcineurin/NFAT, for example, has been identified as one of those responsible for the increase in ventricular mass with predominant increase in interstitial fibrosis, alterations in gene expression and decreased cardiac ventricular function in hypertension. Moreover, other routes, such as the ubiquitin-proteasome system have been less studied in hypertension, remaining doubts about their importance in this disease. Knowing the molecular mechanisms and signaling pathways responsible for pathological cardiac hypertrophy is essential because it will help in the discovery of therapeutic approaches that may inhibit the pathological growth and stimulate the physiological growth. Several studies have shown that the renin angiotensin aldosterone system plays a fundamental role in the development and maintenance of hypertension, since increasing the concentration of angiotensin II (Ang II) that occurs in hypertensive patients, in addition to promoting increased peripheral vascular resistance, contributes directly to cardiac hypertrophy. On the other hand, angiotensin 1-7 [Ang-(1-7)], the other arm of the renin angiotensin system, exerts a cardioprotective effect counter-regulate the effects of Ang II in the heart. In fact, restoring the balance between these two sides of the renin angiotensin system seems to be an important strategy for the treatment of hypertension. Several studies have shown that aerobic exercise training is an extremely important non-pharmacological strategy for the treatment of hypertension. Among the effects of aerobic exercise training in hypertension can highlight the decrease in blood pressure, cardiac remodeling and reverse change of the renin angiotensin aldosterone axis with decreased Ang II and increase Ang-(1-7). However, the mechanisms by which regular exercise provides such benefits are still not known. Moreover, there are doubts about the intensity more suitable to be used in exercise training to obtain benefits of greater magnitude in the treatment of hypertension. Thus, the objectives of this study are (1) to evaluate the role of Ang-(1-7) in reverse remodeling and improves cardiac function in spontaneously hypertensive rats trained and (2) compare the effects of moderate exercise training with the effects of high intensity interval training on function and cardiac remodeling in SHR. The hypothesis of this study is that the reverse cardiac remodeling and improvement of cardiac function provided by exercise training depend on the greater activation of the Ang-(1-7)/receptor MAS as well as the intensity of exercise training. (AU)

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