|Support type:||Scholarships in Brazil - Doctorate|
|Effective date (Start):||January 01, 2016|
|Effective date (End):||September 30, 2018|
|Field of knowledge:||Health Sciences - Medicine - Medical Clinics|
|Principal Investigator:||Antonio Carlos Cicogna|
|Grantee:||Vitor Loureiro da Silva|
|Home Institution:||Faculdade de Medicina (FMB). Universidade Estadual Paulista (UNESP). Campus de Botucatu. Botucatu , SP, Brazil|
Several experimental models have been proposed to study cardiac remodeling (CR); among them, the induction to supravalvar aortic stenosis (SAS). Physiopathological mechanisms responsible for cardiac function depression in this model of study are not well defined, however, there is relation to changes in intracellular calcium transient and their regulatory proteins. Calcium transient is one of the main mechanisms responsible for contraction and relaxation of myocardium; the following proteins modulate flow of intracellular calcium: L-type calcium channel, ryanodine receptor, calsequestrin, sarcoplasmic reticulum calcium pump, phospholamban, sodium/calcium exchanger and sarcolemma calcium pump.Pharmacological and non-pharmacological measures have been employed to promote attenuation of cardiac dysfunction in animals with pathological remodeling. Exercise training is considered a key intervention in preventive cardiology. Specifically, aerobic exercise training (TFa), in normal condition, enhance cardiac function associated to positive adaptations in calcium transient and their regulatory agents. In cardiac pathology motivated, among other factors, for pressure overload, studies show that exercise training restores, total or partially, cardiac function, which delays the transition to heart failure, among other factors, for promoting improvments in intracellular calcium transient of EAo rats. In order to test this premise aired, cardiac function, calcium transient and gene expression of their regulatory proteins of EAo rats submitted to exercise training will be assessed.