Structural alterations in rat myocardium induced by chronic l-arginine and l-NAME supplementation |
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Authors: | Amal Abdussalam Ali A Hmaid Milica Markelic Vesna Otasevic Sava Masovic Aleksandra Jankovic Bato Korac Aleksandra Korac |
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Institution: | 1. Chair of Cell and Tissue Biology, Faculty of Biology, University of Belgrade, Studentski trg 16, 11000 Belgrade, Serbia;2. Department of Physiology, Institute for Biological Research “Sinisa Stankovic”, University of Belgrade, Bulevar Despota Stefana 142, 11000 Belgrade, Serbia |
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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. |
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Keywords: | eNOS endothelial NOS iNOS inducible NOS nNOS neuronal NOS NO nitric oxide NOS nitric oxide synthase Cardiomyocyte Cardiac hypertrophy Myocardium |
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