Short-term exposure to dexamethasone promotes autonomic imbalance to the heart before hypertension.

Hypertension is one of the chronic side effects of dexamethasone (DEX) treatment; however, almost nothing is known about its acute effects. Therefore, the aim of this study was to investigate the possible mechanisms involved in blood pressure control after acute or short-term DEX treatment in adult animals. Eighty Wistar rats were divided into four groups: C1 and C5, for rats treated with saline for 1 or 5 days, respectively; D1 and D5, for rats treated with DEX for 1 or 5 days, respectively (decadron, 1 mg/kg, i.

Exercise attenuates dexamethasone-induced hypertension through an improvement of baroreflex activity independently of the renin-angiotensin system.

Dexamethasone-induced hypertension may be caused by baroreflex alterations or renin-angiotensin system (RAS) exacerbation. Aerobic training has been recommended for hypertension treatment, but the mechanisms responsible for reduction of arterial pressure (AP) in dexamethasone (DEX) treated rats are still inconclusive.This study evaluated whether mechanisms responsible for training-induced attenuation of hypertension involve changes in autonomic nervous system and in RAS components.

Time-course changes of catabolic proteins following muscle atrophy induced by dexamethasone.

This study was designed to describe the time-course changes of catabolic proteins following muscle atrophy induced by 10 days of dexamethasone (DEX). Rats underwent DEX treatment for 1, 3, 5, 7 and 10 days. Body weight (BW) and lean mass were obtained using a dual energy X-ray absorptiometry (DEXA) scan.