Author: Korsager Larsen M1, Matchkov VV2.
Affiliation: 1Department of Biomedicine, Faculty of Health, Aarhus University, Aarhus, Denmark. 2Department of Biomedicine, Faculty of Health, Aarhus University, Aarhus, Denmark. Electronic address: vvm@biomed.au.dk.
Conference/Journal: Medicina (Kaunas).
Date published: 2016
Other:
Volume ID: 52 , Issue ID: 1 , Pages: 19-27 , Special Notes: doi: 10.1016/j.medici.2016.01.005. Epub 2016 Jan 29. , Word Count: 231
Oxidative stress is associated with the pathogenesis of hypertension. Decreased bioavailability of nitric oxide (NO) is one of the mechanisms involved in the pathogenesis. It has been suggested that physical exercise could be a potential non-pharmacological strategy in treatment of hypertension because of its beneficial effects on oxidative stress and endothelial function. The aim of this review is to investigate the effect of oxidative stress in relation to hypertension and physical exercise, including the role of NO in the pathogenesis of hypertension. Endothelial dysfunction and decreased NO levels have been found to have the adverse effects in the correlation between oxidative stress and hypertension. Most of the previous studies found that aerobic exercise significantly decreased blood pressure and oxidative stress in hypertensive subjects, but the intense aerobic exercise can also injure endothelial cells. Isometric exercise decreases normally only systolic blood pressure. An alternative exercise, Tai chi significantly decreases blood pressure and oxidative stress in normotensive elderly, but the effect in hypertensive subjects has not yet been studied. Physical exercise and especially aerobic training can be suggested as an effective intervention in the prevention and treatment of hypertension and cardiovascular disease via reduction in oxidative stress.
Copyright © 2016 The Lithuanian University of Health Sciences. Production and hosting by Elsevier Urban & Partner Sp. z o.o. All rights reserved.
KEYWORDS: Exercise; Hypertension; Nitric oxide; Oxidative stress; Redox state
PMID: 26987496 [PubMed - in process]