Volume 37, Issue 2 (8-2013)                   Research in Medicine 2013, 37(2): 73-80 | Back to browse issues page

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Associate Professor in Physiology, Endocrine Physiology Research Center, Research Institute for Endocrine Sciences, Shahid Beheshti University of Medical Sciences, Tehran, Iran
Abstract:   (10239 Views)
Abstract Background: Reduced Nitric oxide (NO) synthesis has been reported in hypothyroidism. NO has many physiological and pathological roles. The purpose of this study was to determine NO metabolites, nitrate and nitrite (NOx), levels in serum and tissues of heart, brain, cerebellum and aorta of rats with fetal hypothyroidism. . Materials and methods: Hypothyroidism was induced in female rats using 6-n-propylthiouracil in drinking water from beginning to the end of gestation. Male offsprings of the control and experimental groups (with induced hypothyroidism) were kept under observation until adulthood and divided into four groups (n=9 in each group): control and experimental groups who were administered L-arginine (2%) and control and experimental groups without L-arginine. NOx concentrations in serum and tissue samples were analyzed using Griess method. Results: NOx concentrations in the heart, brain, cerebellum and aortic tissue of the experimental group were significantly lower than the control group. After 1 week of L-arginine administration, NOx concentrations in the heart, brain, cerebellum and serum decreased in the control group while in aortic and liver tissue it was immeasurable. In the rats with fetal hypothyroidism NOx concentrations decreased in serum and aorta but showed a significant increase in the cerebellar tissue. Conclusion: NOx metabolism in hypothyroidism is different from controls and thyroid hormones have an effect on NOx metabolism. Increasing extracellular L-arginine concentration alters NOx concentration in serum and tissues. Keywords: Fetal hypothyroidism, Nitric oxide, L-arginine, Rat.
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Type of Study: Original |
Received: 2013/10/29 | Accepted: 2017/12/12 | Published: 2017/12/12