Pregnancy is characterized by insulin resistance that is associated with increased angiotensin II (AngII) and insulin levels. Therefore, pregnancy may change insulin-induced vasodilation through changes in AngII receptors. Insulin-induced vasorelaxation… Click to show full abstract
Pregnancy is characterized by insulin resistance that is associated with increased angiotensin II (AngII) and insulin levels. Therefore, pregnancy may change insulin-induced vasodilation through changes in AngII receptors. Insulin-induced vasorelaxation was evaluated in phenylephrine-precontracted aortic rings of pregnant and non-pregnant rats, using a conventional isolated organ preparation. Experiments were performed in thoracic or abdominal aorta rings with or without endothelium in the presence and absence of L-NAME (10-5 M), losartan (10-7 M) or PD123319 (10-7 M). AT1 and AT2 receptors expression were detected by immunohistochemistry. Insulin-induced vasodilation was endothelium and NO dependent and decreased in the thoracic aorta but increased in the abdominal segment of pregnant rats. Insulin's vasorelaxant effect was increased by losartan mainly on the thoracic aorta. PD123319 decreased insulin-induced vasorelaxation mainly in the pregnant rat abdominal aorta. AT1 receptors' expression was decreased while AT2 receptors' expression was increased by pregnancy. In conclusion, pregnancy changes insulin-induced vasorelaxation. Moreover, insulin vasodilation is tonically inhibited by AT1 receptors, while AT2 receptors appear to have an insulin-sensitizing effect. The role of pregnancy and AngII receptors differ depending on the aorta segment. These results shed light on the role of pregnancy and AngII receptors on the regulation of insulin-mediated vasodilation.
               
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