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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Angiotensin II promotes iron accumulation and depresses PGI 2 and NO synthesis in endothelial cells: Effects of losartan and propranolol analogs
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Angiotensin II promotes iron accumulation and depresses PGI 2 and NO synthesis in endothelial cells: Effects of losartan and propranolol analogs

机译：血管紧张素II促进铁积累并抑制内皮细胞中的PGI 2和NO合成：氯沙坦和普萘洛尔类似物的作用

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摘要

Angiotensin may promote endothelial dysfunction through iron accumulation. To research this, bovine endothelial cells (ECs) were incubated with iron (30 μmol·L -1) with or without angiotensin II (100 nmol·L -1). After incubation for 6 h, it was observed that the addition of angiotensin enhanced EC iron accumulation by 5.1-fold compared with a 1.8-fold increase for cells incubated with iron only. This enhanced iron uptake was attenuated by losartan (100 nmol·L -1), D-propranolol (10 μmol·L -1), 4-HO-propranolol (5 μmol·L -1), and methylamine, but not by vitamin E or atenolol. After 6 h of incubation, angiotensin plus iron provoked intracellular oxidant formation (2'7'-dichlorofluorescein diacetate (DCF-DA) fluorescence) and elevated oxidized glutathione; significant loss of cell viability occurred at 48 h. Stimulated prostacyclin release decreased by 38% (6 h) and NO synthesis was reduced by 41% (24 h). Both oxidative events and functional impairment were substantially attenuated by losartan or D-propranolol. It is concluded that angiotensin promoted non-transferrinbound iron uptake via AT-1 receptor activation, leading to EC oxidative functional impairment. The protective effects of D-propranolol and 4-HO-propranolol may be related to their lysosomotropic properties.
机译：血管紧张素可能通过铁的积累促进内皮功能障碍。为了对此进行研究，将牛内皮细胞（ECs）与含或不含血管紧张素II（100nmol·L-1）的铁（30μmol·L-1）一起孵育。温育6小时后，观察到血管紧张素的添加使EC铁的蓄积增加了5.1倍，而仅用铁温育的细胞则增加了1.8倍。氯沙坦（100nmol·L-1），D-普萘洛尔（10μmol·L-1），4-HO-普萘洛尔（5μmol·L-1）和甲胺会减弱铁的吸收，但维生素不会E或阿替洛尔。温育6小时后，血管紧张素加铁引起细胞内氧化剂的形成（2'7'-二氯荧光素二乙酸盐（DCF-DA）荧光）并升高了氧化型谷胱甘肽;在48 h时细胞活力明显下降。刺激的前列环素释放减少38％（6小时），NO合成减少41％（24小时）。氯沙坦或D-普萘洛尔可大大减弱氧化事件和功能损害。结论是，血管紧张素通过AT-1受体激活促进非转铁蛋白结合的铁摄取，从而导致EC氧化功能受损。 D-普萘洛尔和4-HO-普萘洛尔的保护作用可能与它们的溶同溶性有关。

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