Role of renin-antiotensin-system and simpathetic nervous system in dexamethasone-induced hypertension: preventive effects of exercise training

• Grant number: 11/21522-0
• Support Opportunities: Regular Research Grants
• Start date: February 01, 2012
• End date: July 31, 2014
• Field of knowledge: Health Sciences - Physical Education
• Principal Investigator: Sandra Lia do Amaral Cardoso
• Grantee: Sandra Lia do Amaral Cardoso
• Host Institution: Faculdade de Ciências (FC). Universidade Estadual Paulista (UNESP). Campus de Bauru. Bauru , SP, Brazil
• Associated researchers: Carlos Ferreira dos Santos

Abstract

Synthetic glucocorticoids are widely used nowadays in order to treat inflammation and allergies. However, the chronic use may determine metabolic and haemodynamic alterations causing diabetes, dyslipidemia and hypertension. It has been shown that the excess of glucocorticoids causes increases in blood pressure, however, the mechanisms responsible by this effect are not completely known. It is known that renin-angiotensin system (RAS) and sympathetic nervous system (SNS) contribute to the development/maintenance of essential hypertension in men and in different experimental models of hypertension. Aerobic exercise, on the other hand, is used as part of treatment since it promotes central and peripheral adaptive responses. We have shown that pre-physical conditioning attenuates high level of blood pressure, as well as hyperglycemia and hiperinsulinemia followed by dexamethasone treatment (Amaral et a, 2010 and Barel et al, 2010). However, almost nothing is known about the role of RAS and SNS on hypertension induced by dexamethasone. This work investigates if the mechanisms induced by exercise training to decrease blood pressure involve the RAS and/or SNS. Wistar rats, sedentary and trained, treated or not, will be used. After the determination of fasting glycemia, basal blood pressure and the response to hexamethonium, the rats will be anesthetized in order to have their skeletal and cardiac muscles harvested and processed for genes and protein related to the RAS determination. (AU)

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)

KRUG, ANDRE L. O.; MACEDO, ANDERSON G.; ZAGO, ANDERSON S.; RUSH, JAMES W. E.; SANTOS, CARLOS F.; AMARAL, SANDRA L.. High-intensity resistance training attenuates dexamethasone-induced muscle atrophy. MUSCLE & NERVE, v. 53, n. 5, p. 779-788, MAY 2016. (12/21820-3, 11/21522-0)

FLEURY, CAMILA A.; ANDREO, VAGNER C.; LOMBA, PEDRO C.; DIONISIO, THIAGO J.; AMARAL, SANDRA L.; SANTOS, CARLOS F.; FARIA, FLAVIO A.. Comparison of epinephrine and felypressin pressure effects in 1K1C hypertensive rats treated or not with atenolol. JOURNAL OF ANESTHESIA, v. 29, n. 1, p. 56-64, FEB 2015. (11/21522-0)

MACEDO, ANDERSON G.; KRUG, ANDRE LUIS O.; SOUZA, LIDIANE M.; MARTUSCELLI, ALINE M.; CONSTANTINO, PAULA B.; ZAGO, ANDERSON S.; RUSH, JAMES W. E.; SANTOS, CARLOS F.; AMARAL, SANDRA L.. Time-course changes of catabolic proteins following muscle atrophy induced by dexamethasone. Steroids, v. 107, p. 30-36, MAR 2016. (12/21820-3, 11/21522-0)

CONSTANTINO, PAULA B.; DIONISIO, THIAGO J.; DUCHATSCH, FRANCINE; HERRERA, NAIARA A.; DUARTE, JOSIANE O.; SANTOS, CARLOS F.; CRESTANI, CARLOS C.; AMARAL, SANDRA L.. Exercise attenuates dexamethasone-induced hypertension through an improvement of baroreflex activity independently of the renin-angiotensin system. Steroids, v. 128, p. 147-154, DEC 2017. (14/23050-6, 12/19722-3, 12/14376-0, 11/21522-0, 14/18177-7)

MACEDO, ANDERSON G.; KRUG, ANDRE L. O.; HERRERA, NAIARA A.; ZAGO, ANDERSON S.; RUSH, JAMES W. E.; AMARAL, SANDRA L.. Low-intensity resistance training attenuates dexamethasone-induced atrophy in the flexor hallucis longus muscle. JOURNAL OF STEROID BIOCHEMISTRY AND MOLECULAR BIOLOGY, v. 143, p. 357-364, SEP 2014. (12/21820-3, 11/21522-0)