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. 2014:2014:703175.
doi: 10.1155/2014/703175. Epub 2014 Jul 6.

Hypertension and cardiovascular remodelling in rats exposed to continuous light: protection by ACE-inhibition and melatonin

Affiliations

Hypertension and cardiovascular remodelling in rats exposed to continuous light: protection by ACE-inhibition and melatonin

Fedor Simko et al. Mediators Inflamm. 2014.

Abstract

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.

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Figures

Figure 1
Figure 1
The influence of captopril (24C) and melatonin (24M) on blood pressure (a) and relative left ventricle (LV) weight (LVW/BW) (b) in 24 hours/day continuous light exposure-induced hypertension (24). c: Wistar controls. *P < 0.05 versus c; # P < 0.05 versus 24.
Figure 2
Figure 2
The influence of captopril (24C) and melatonin (24M) on wall thickness (a) and cross-sectional area (b) of the aorta in 24 hours/day continuous light exposure-induced hypertension (24). c: Wistar controls. *P < 0.05 versus c; # P < 0.05 versus 24.
Figure 3
Figure 3
The influence of captopril (24C) and melatonin (24M) on hydroxyproline concentration in soluble (a) and insoluble (b) collagen proteins and on total hydroxyproline concentration (c) in 24 hours/day continuous light exposure-induced hypertension (24). c: Wistar controls. *P < 0.05 versus c; # P < 0.05 versus 24.
Figure 4
Figure 4
The influence of captopril (24C) and melatonin (24M) on advanced oxidation protein products (AOPP) in the LV (a) and aorta (b) and on advanced glycation end-products (AGEs) in the LV (c) and in the aorta (d) in 24 hours/day continuous light exposure-induced hypertension (24). c: Wistar controls. *P < 0.05 versus c; # P < 0.05 versus 24.
Figure 5
Figure 5
The influence of captopril (24C) and melatonin (24M) on wall thickness of aorta stained by hematoxylin-eosin in 24 hours/day continuous light exposure-induced hypertension (24). c: Wistar controls.
Figure 6
Figure 6
The influence of captopril (24C) and melatonin (24M) on the concentration of collagen I (a), III (b), and the sum of collagens I and III (c) in the aortic media in 24 hours/day continuous light exposure-induced hypertension (24). c: Wistar controls. *P < 0.05 versus c; # P < 0.05 versus 24 (according to [36] with permission).
Figure 7
Figure 7
The influence of captopril (24C) and melatonin (24M) on the concentration of collagen in the aortic media in 24 hours/day continuous light exposure-induced hypertension (24). Specimens are stained with picrosirius red and evaluated in polarized light: red to yellow color represents collagen I and green color represents collagen III. c: Wistar controls (according to [36] with permission).

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