Abstract
The exact mechanism by which Endothelin-1 (ET-1), Angiotensin II (Ang II), and their antagonists act in physiology are controversial subjects among researchers, therefore the present work aimed to investigate the effects of bosentan and losartan on oxidative stress and serum cortisol level in rats. This study includes two experiments. The first one included four groups: The first group treated with saline, the second group treated with ET-1 , the third group treated with Bosentan + ET-1, and the fourth group treated with Losartan + ET-1. The second experiment also included four groups: The first group treated with saline, the second group treated with Ang II , the third group treated with Losartan + Ang II, and the fourth group treated with Bosentan + Ang II. The results demonstrate that, bolus infusion of losartan significantly decreased serum cortisol level versus ET-1. Bosentan significantly decreased cortisol level compared with Ang II infusion. Neither losartan nor Ang II changed serum cortisol significantly versus Ang II and saline groups. Furthermore, bosentan caused rising in malondialdehyde (MDA) concentration compared to ET-1 infusion, but losartan slightly decreased it. MDA in Ang II infusion dramatically became high in comparison with saline infusion, and both losartan. Serum glucose concentration clearly rose in losartan infusion, while bosentan did affect it significantly. Serum chloride in both bosentan and losartan significantly increased compared to ET-1. Both ET-1 and Ang II infusions for one hour led to increasing Mg++ concentration versus saline infusion. In conclusion, both ET-1 and Ang II antagonists reduced cortisol level , but they did not change lipid peroxidation marker as elevated by Ang II infusion. Interestingly, ET-1 and Ang II markedly could increase serum Mg++ levels, but their antagonists did not return it to the normal levels.
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