Sección de Estudios de Posgrado e Investigación, Escuela Superior de Medicina, Instituto Politécnico Nacional, Ciudad de México 11340, México.
Can J Physiol Pharmacol. 2021 Oct;99(10):1026-1035. doi: 10.1139/cjpp-2021-0057. Epub 2021 Apr 15.
Insulin resistance is a feature of pregnancy and is associated with increased levels of angiotensin II (Ang II) and insulin. Therefore, pregnancy may change insulin-induced vasodilation through changes in Ang II 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 N-nitro-L-arginine methyl ester (L-NAME) (10 M), losartan (10 M), or PD123319 (10 M). AT1 and AT2 receptor expressions were detected by immunohistochemistry. Insulin-induced vasodilation was endothelium- and nitric oxide-dependent and decreased in the thoracic aorta but increased in the abdominal segment of pregnant rats. The 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 receptor expression was decreased while AT2 receptor 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 Ang II receptors differ depending on the aorta segment. These results shed light on the role of pregnancy and Ang II receptors on the regulation of insulin-mediated vasodilation.
胰岛素抵抗是妊娠的一个特征，与血管紧张素 II（Ang II）和胰岛素水平升高有关。因此，妊娠可能通过 Ang II 受体的变化改变胰岛素诱导的血管舒张。使用传统的离体器官制备，评估了妊娠和非妊娠大鼠去甲肾上腺素预收缩的胸主动脉环中胰岛素诱导的血管舒张。在存在和不存在 N-硝基-L-精氨酸甲酯（L-NAME）（10 μM）、洛沙坦（10 μM）或 PD123319（10 μM）的情况下，在有或没有内皮的情况下进行了胸主动脉或腹主动脉环的实验。通过免疫组织化学检测 AT1 和 AT2 受体表达。胰岛素诱导的血管舒张是内皮依赖性和一氧化氮依赖性的，在胸主动脉中减少，但在妊娠大鼠的腹主动脉段中增加。洛沙坦主要在胸主动脉上增加了胰岛素的血管舒张作用。PD123319 主要降低了妊娠大鼠腹主动脉中胰岛素诱导的血管舒张作用。AT1 受体表达减少，而 AT2 受体表达增加。总之，妊娠改变了胰岛素诱导的血管舒张。此外，AT1 受体对胰岛素诱导的血管舒张具有紧张性抑制作用，而 AT2 受体似乎具有胰岛素增敏作用。妊娠和 Ang II 受体的作用因主动脉段而异。这些结果阐明了妊娠和 Ang II 受体在调节胰岛素介导的血管舒张中的作用。
