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Physical training effects on hypertension, arterial stiffness and muscle atrophy induced by dexamethasone: role of oxidative stress

Abstract

Dexamethasone (DEX) is widely used in clinics due to its potent effect as anti-allergic and anti-inflammatory drug, however its chronic use may cause several metabolic and haemodynamic alterations. It has been shown that DEX treatment provokes hypertension and muscle atrophy, however the mechanisms responsible for these effects are not totally understood. We recently have shown that renin-angiotensin system maybe not the main contributor for DEX- induced hypertension. On the other hand, reactive oxygen species (ROS) seems to be a common mechanism for hypertension and muscle atrophy but its involvement in hypertension and muscle atrophy induced by DEX needs to be investigated. Physical training has been considered a potent strategy in controlling hypertension and muscular atrophy, however, if its effects includes a better balance between ROS and anti-oxidant enzymes are not known. Therefore the main purpose of this study is to investigate if hypertension and muscle atrophy induced by DEX occurs due to an imbalance between production and removal of ROS and if the physical exercise attenuation of these side-effects involves an improvement on redox-balance. To answer these questions this study will associate functional (blood pressure and arterial stiffness) and structural (wall-to-lumen ratio and fibers transverse area section) techniques. These parameters will be associated with molecular evaluations, both gene expression and protein levels of mechanisms responsible for redox-status and muscle atrophy in sedentary and trained rats, treated or not with DEX. (AU)

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Scientific publications (5)
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
JESUS, ISLEY; HERRERA, NAIARA A.; ANDREO, JESUS C.; SANTOS, CARLOS F.; AMARAL, SANDRA L. Training counteracts DEX-induced microvascular rarefaction by improving the balance between apoptotic and angiogenic proteins. Steroids, v. 156, APR 2020. Web of Science Citations: 0.
FABRICIO, MAYARA F.; JORDAO, MARIA T.; MIOTTO, DANYELLE S.; RUIZ, THALLES F. R.; VICENTINI, CARLOS A.; LACCHINI, SILVIA; SANTOS, CARLOS FERREIRA; MICHELINI, LISETE C.; AMARAL, SANDRA L. Standardization of a new non-invasive device for assessment of arterial stiffness in rats: Correlation with age-related arteries' structure. METHODSX, v. 7, 2020. Web of Science Citations: 2.
DUCHATSCH, FRANCINE; CONSTANTINO, PAULA B.; HERRERA, NAIARA A.; FABRICIO, MAYARA F.; TARDELLI, LIDIELI P.; MARTUSCELLI, ALINE M.; DIONISIO, THIAGO J.; SANTOS, CARLOS F.; AMARAL, SANDRA L. Short-term exposure to dexamethasone promotes autonomic imbalance to the heart before hypertension. JOURNAL OF THE AMERICAN SOCIETY OF HYPERTENSION, v. 12, n. 8, p. 605-613, AUG 2018. Web of Science Citations: 0.
HERRERA, NAIARA A.; JESUS, ISLEY; DIONISIO, EVANDRO J.; DIONISIO, THIAGO J.; SANTOS, CARLOS F.; AMARAL, SANDRA L. Exercise Training Prevents Dexamethasone-induced Rarefaction. Journal of Cardiovascular Pharmacology, v. 70, n. 3, p. 194-201, SEP 2017. Web of Science Citations: 2.
HERRERA, NAIARA A.; JESUS, ISLEY; SHINOHARA, ANDRE L.; DIONISIO, THIAGO J.; SANTOS, CARLOS F.; AMARAL, SANDRA L. Exercise training attenuates dexamethasone-induced hypertension by improving autonomic balance to the heart, sympathetic vascular modulation and skeletal muscle microcirculation. Journal of Hypertension, v. 34, n. 10, p. 1967-1976, OCT 2016. Web of Science Citations: 4.

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