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Current Trends in Endocrinology   Volumes    Volume 8 
Salt intake and renal inflammatory factors: Modulatory role of thyroid hormone
Andrés Quesada, Sebastián Montoro-Molina, Pablo Vargas-Tendero, Ángela García-Tendero, Félix Vargas
Pages: 45 - 53
Number of pages: 9
Current Trends in Endocrinology
Volume 8 

Copyright © 2016 Research Trends. All rights reserved

This study assessed the effects of changes in saline intake on renal cortex inflammatory cytokines (interleukin 6 (IL6), tumour necrosis factor alpha (TNF-α) and vascular endothelial growth factor (VEGF)) and hemodynamic, morphologic, and plasma variables in experimental thyroid disorders. In the present study, eight groups of male Wistar rats were used: euthyroid, hypothyroid, and hyperthyroid groups on a diet of normal salt (0.4% NaCl); the same groups on a high salt diet (8% via food intake); and euthyroid and hyperthyroid groups on a low salt (0.02%) diet. Blood pressure (BP) and heart rate were directly recorded, and the morphologic, plasma and renal variables were measured. BP increased and decreased in hyper- and hypothyroid rats, respectively. BP increased with high salt treatment and decreased with low salt intake in hyperthyroid rats but did not change in euthyroid or hypothyroid rats. The levels of all renal cortex inflammatory cytokines significantly decreased in hypothyroid rats but did not change in hyperthyroid rats. High salt diet reduced the levels of all renal inflammatory cytokines in euthyroid and hyperthyroid rats, and the reduction was significant. Low salt diet increased the inflammatory cytokine levels in renal cortex of euthyroid rats. In summary, this study demonstrates that: (i) salt intake is inversely related to renal inflammatory variables; (ii) the salt-sensitive model of hypertension induced by hyperthyroidism is not accompanied by an increase in renal inflammatory cytokines and (iii) hypothyroidism is associated with a reduction in inflammatory cytokines in renal tissues, which might contribute to its protective effects against renal injury.
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