Efeitos do treinamento físico combinado na rigidez arterial de ratos tratados com dexametasona
Paula, Vinicius Ferreira de
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Arterial stiffness, determined by pulse wave velocity (PWV) has been considered an important cardiovascular risk predictor. It has been shown that high arterial stiffness contributes to develop hypertension (HT) and may be determined by an unbalance between the main extracellular proteins, like collagen and elastin. Previous studies have demonstrated that dexamethasone (DEX) increases arterial pressure (AP) in rats and humans; however the DEX effects on arterial stiffness are unclear. On the other hand, combined physical training (CT) has been recommended to control hypertension, but almost nothing is known about its effects on mechanisms responsible to control arterial stiffness. We hypothesized that CT could control collagen and elastin levels and attenuate arterial stiffness and AP increase in DEX-treated rats. Therefore, the aim of this study was to evaluate the effects of CT on arterial stiffness and AP in DEX-treated rats. Thirty-seven Wistar rats (200-250g) were allocated into 4 groups: sedentary control (SC, n = 8), sedentary treated with DEX (SD, n = 9), trained control (TC, n=10) and trained and treated with DEX (TD, n = 10). All rats performed a maximum voluntary carrying capacity test (MVCC, on the ladder) and a maximal physical capacity test (TEM, on the treadmill) and underwent CT (60% maximum, 5d / week, 1h / on alternate days, for 74 days) or were kept sedentary. Through the last 14 days, they were treated with DEX (50μg / kg per day, s.c.) or saline. At the end experimental protocol, rats underwent pulse wave velocity (PWV) and tail AP measurements. Two-way ANOVA and T-Student t-test were used to compare the groups. Tukey post-hoc test was used when necessary. Maximal physical capacity test or MVCC values, PWV and AP were correlated by Pearson/Spearman test (p <0.05). Trained rats showed higher responses on MVCC and TEM compared with sedentary rats. DEX treatment increased tail AP (from 116 ± 2 to 181 ± 5 mmHg, p <0.05) as well as VOP (from 1.5 ± 0.05 m/s to 2.1 ± 0 m/s). On the other hand, TD group presented attenuation of AP and PWV increase induced by DEX (11% and 7.3%, for AP and PWV, respectively) when compared with SD group (53% e 38%, for AP and PWV, respectively). Also, DEX treatment increased COL III protein levels (+51,62%) in SD and CT significantly attenuated this increase (TD, +4,31%). COL I/COL III was significantly reduced after DEX treatment. Ellastin levels were not altered. Results of PWV were associated with AP (r = 0.6714) as well as COL III (r=0.4567). Therefore, the results of the present study are unique in demonstrating that CT was able mitigate increase on arterial stiffness induced by DEX treatment and the mechanism may involve a better control of aorta COL III levels. This CT-induced PWV attenuation may contribute to the lower AP observed in trained DEX-treated rats.