Please use this identifier to cite or link to this item: https://biore.bio.bg.ac.rs/handle/123456789/106
Title: Structural alterations in rat myocardium induced by chronic L-arginine and L-NAME supplementation
Authors: Hmaid, Amal Abdussalam Ali A.
Markelić, Milica 
Otasevic, Vesna
Masovic, Sava
Jankovic, Aleksandra
Korać, Bato 
Korać, Aleksandra 
Keywords: Cardiac hypertrophy;Cardiomyocyte;L-Arginine;L-NAME;Myocardium
Issue Date: 1-Mar-2018
Rank: M21
Project: White or/and brown: importance of adipose tissue in overall redox dependent metabolic control in physiological adaptations and metabolic disorders 
Journal: Saudi Journal of Biological Sciences
Abstract: 
Structural changes affecting cardiomyocyte function may contribute to the pathophysiological remodeling underlying cardiac function impairment. Recent reports have shown that endogenous nitric oxide (NO) plays an important role in this process. In order to examine the role of NO in cardiomyocyte remodeling, male rats were acclimated to room temperature (22 ± 1 °C) or cold (4 ± 1 °C) and treated with 2.25% L-arginine·HCl or 0.01% L-NAME (Nω-nitro-L-arginine methyl ester)·HCl for 45 days. Untreated groups served as controls. Right heart ventricles were routinely prepared for light microscopic examination. Stereological estimations of volume densities of cardiomyocytes, surrounding blood vessels and connective tissue, as well as the morphometric measurements of cardiomyocyte diameters were performed. Tissue sections were also analyzed for structural alterations. We observed that both L-arginine and L-NAME supplementation induced cardiomyocyte hypertrophy, regardless of ambient temperature. However, cardiomyocyte hypertrophy was associated with fibrosis and extra collagen deposition only in the L-NAME treated group. Taken together, our results suggest that NO has a modulatory role in right heart ventricle remodeling by coordinating hypertrophy of cardiomyocytes and fibrous tissue preventing cardiac fibrosis.
URI: https://biore.bio.bg.ac.rs/handle/123456789/106
ISSN: 1319-562X
DOI: 10.1016/j.sjbs.2016.01.022
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