Swimming training prevents coronary endothelial dysfunction in ovariectomized spontaneously hypertensive rats

Abstract

Estrogen deficiency and hypertension are considered major risk factors for the development of coronary heart disease. On the other hand, exercise training is considered an effective form to prevent and treat cardiovascular diseases. However, the effects of swimming training (SW) on coronary vascular reactivity in female ovariectomized hypertensive rats are not known. We aimed to evaluate the effects of SW on endothelium-dependent coronary vasodilation in ovariectomized hypertensive rats. Three-month old spontaneously hypertensive rats (SHR, n=50) were divided into four groups: sham (SH), sham plus swimming training (SSW), ovariectomized (OVX), and ovariectomized plus swimming training (OSW). The SW protocol (5 times/week, 60 min/day) was conducted for 8 weeks. The vasodilatory response was measured in isolated hearts in the absence and presence of a nitric oxide synthase inhibitor (L-NAME, 100 µM). Cardiac oxidative stress was evaluated in situ by dihydroethidium fluorescence, while the expression of antioxidant enzymes (SOD-2 and catalase) and their activities were assessed by western blotting and spectrophotometry, respectively. Vasodilation in SHR was significantly reduced by OVX, even in the presence of L-NAME, in conjunction with an increased oxidative stress. These effects were prevented by SW, and were associated with a decrease in oxidative stress. Superoxide dismutase 2 (SOD-2) and catalase expression increased only in the OSW group. However, no significant difference was found in the activity of these enzymes. In conclusion, SW prevented the endothelial dysfunction in the coronary bed of ovariectomized SHR associated with an increase in the expression of antioxidant enzymes, and therefore may prevent coronary heart disease in hypertensive postmenopausal women.

Exercise intervention attenuates hyperhomocysteinemia-induced aortic endothelial oxidative injury by regulating SIRT1 through mitigating NADPH oxidase/LOX-1 signaling

“…Exercise training has been used as an important therapeutic intervention against cardiovascular diseases [19] , and regular exercise has been shown to have beneficial effects on the cardiovascular system [20] . Claudio et al suggested that regular exercise protects against ovariectomy-induced coronary endothelial dysfunction by repressing oxidative stress [21] . Our group previously found that the activation of SIRT1 function protected against Hcy-induced endothelial apoptosis and oxidative stress [9] .…”

Is 3 Weeks of Exercise Enough to Change Blood Pressure and Cardiac Redox State in Hypertensive Rats?

“…According to Claudio et al excercise training prevented the increase of ROS production in ovariectomized hypertensive rats demonstrating increased expresion of antioxidative enzymes. Potential explanation for non excessive production of ROS besides above mentioned mechanism, may also be lower electron leakage from mitochondria or chronic exposure of tissue to ROS, induced by training, which makes the organ more resistant to the effects that derive from the mechanisms of oxidative stress (37).…”

Cardiovascular Benefits of Exercise Training in Postmenopausal Hypertension

“…Women’s weight gain after menopause is a well-recognized phenomenon which is accompanied by a multitude of changes in body composition [ 13 ]. Significant increase in the gain of body weight was observed in hypertensive rats after ovariectomy [ 14 , 15 , 16 ]. Epicardial fat is positively associated with obesity and body mass index (BMI).…”

“…Increased oxidative stress is a common feature in the pathogenesis of arterial hypertension and postmenopause. Excessive oxidative stress has been observed in rat myocardium and coronary endothelial dysfunctions in hypertensive ovariectomy, suggesting that these impaired mechanisms may reflect a worsening heart failure in hypertensive postmenopausal women [ 14 , 31 ]. Reactive oxygen species (ROS) are implicated in the pathogenesis of cardiovascular disease such as hypertension, atherosclerosis, myocardial infarction, and cardiac failure.…”

“…ROS can directly damage the lipids of cell membranes, proteins, and both nuclear and mitochondrial DNA, all of which result in serious or mortal cellular injury. However, several studies have demonstrated that vasodilation could be enhanced indirectly after exercise training by a distinct mechanism to increase antioxidant biomarkers such as superoxide dismutase (SOD) and catalase activities [ 14 , 35 ]. In human studies, eight weeks of treadmill aerobic exercise training promoted a profound increase in SOD activity in about 86.6% of hypertensive postmenopausal women [ 22 ].…”