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Mediators of Inflammation
Volume 2014 (2014), Article ID 703175, 10 pages
Research Article

Hypertension and Cardiovascular Remodelling in Rats Exposed to Continuous Light: Protection by ACE-Inhibition and Melatonin

1Department of Pathophysiology, School of Medicine, Comenius University, Sasinkova 4, 81372 Bratislava, Slovakia
23rd Clinic of Medicine, School of Medicine, Comenius University, 83305 Bratislava, Slovakia
3Institute of Experimental Endocrinology, Slovak Academy of Sciences, 83305 Bratislava, Slovakia
4Center of Excellence NOREG, 81372 Bratislava, Slovakia
5Institute of Normal and Pathological Physiology, Slovak Academy of Sciences, 81371 Bratislava, Slovakia
6Institute of Molecular Biomedicine, School of Medicine, Comenius University, 81372 Bratislava, Slovakia
7Department of Physiology, School of Medicine, Charles University, 50038 Hradec Kralove 1, Czech Republic

Received 10 January 2014; Revised 27 May 2014; Accepted 29 May 2014; Published 6 July 2014

Academic Editor: Russel J. Reiter

Copyright © 2014 Fedor Simko et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Exposure of rats to continuous light attenuates melatonin production and results in hypertension development. This study investigated whether hypertension induced by continuous light (24 hours/day) exposure induces heart and aorta remodelling and if these alterations are prevented by melatonin or angiotensin converting enzyme inhibitor captopril. Four groups of 3-month-old male Wistar rats (10 per group) were treated as follows for six weeks: untreated controls, exposed to continuous light, light-exposed, and treated with either captopril (100 mg/kg/day) or melatonin (10 mg/kg/day). Exposure to continuous light led to hypertension, left ventricular (LV) hypertrophy and fibrosis, and enhancement of the oxidative load in the LV and aorta. Increase in systolic blood pressure by continuous light exposure was prevented completely by captopril and partially by melatonin. Both captopril and melatonin reduced the wall thickness and cross-sectional area of the aorta and reduced the level of oxidative stress. However, only captopril reduced LV hypertrophy development and only melatonin reduced LV hydroxyproline concentration in insoluble and total collagen in rats exposed to continuous light. In conclusion, captopril prevented LV hypertrophy development in the continuous light-induced hypertension model, while only melatonin significantly reduced fibrosis. This antifibrotic action of melatonin may be protective in hypertensive heart disease.