Abstract
Stress has emerged as a factor associated with cardiovascular disease. Catecholamines released during the stress reaction by the sympathetic nerves and the adrenal medulla couple to β1-and β2-adrenoceptors in the cardiomyocytes membrane enhancing heart function in order to attend the organism demand. This might produce excessive reactive oxygen species what may culminate with oxidative stress and progression of several cardiac diseases. Sirtuins have been described as cardioprotective factors and important regulators of the cellular stress response in the heart. The aim of this work is to investigate the putative participation of oxidative stress and sirtuins in the heart of rats submitted to foot shock stress, an experimental model where there is up regulation of β2-adrenoceptors and downregulation of β1-adrenoceptors. The data have shown that in the myocardium of rats submitted to foot shock stress the H2O2 concentration, catalase and superoxide dismutase activity, NAD+/NADH ratio, as well as the protein expression of sirtuins 1 and 3 were not altered. Pharmacological blockade of the β2-adrenoceptors by ICI118,551, did not modify this scenario. It is concluded that foot shock stress does not cause disruptions in oxidative stress or redox state processes in the myocardium, and consequently, sirtuins are not recruited to stress response.
Highlights
Stress is the body response to any challenge or threat aimed to guarantee survival in adversity
As a result of the increased heart beating and developed force, there is an increase of cardiomyocytes metabolism and production of reactive oxygen reduced levels of sirtuin 3 (SIRT3) were reported in failing hearts and in cardiac fibrosis and contractile dysfunction [15,17,18]
In order to explore the balance of oxidative stress in the cardiac tissue post foot shock stress, H2O2 production and antioxidant enzymes activity were evaluated
Summary
Stress is the body response to any challenge or threat aimed to guarantee survival in adversity. Β1/β2-AR ratio is altered in various experimental models of stress [1,2,3,4,5]. In the foot shock stress model such alteration is due to downregulation of β1-AR and upregulation of β2-AR [4,6]. Once activated, those receptors trigger intracellular signaling cascades that modulate cardiomyocytes life cycle as well as cardiac function [1]. As a result of the increased heart beating and developed force, there is an increase of cardiomyocytes metabolism and production of reactive oxygen reduced levels of SIRT3 were reported in failing hearts and in cardiac fibrosis and contractile dysfunction [15,17,18]. SIRT1 expression seems to play a protective role in cardiomyocytes due the apoptosis inhibition and the expression of FoxOdependent antioxidants enzymes [19,20,21,22]
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