Glucocorticoid-induced vascular endothelial dysfunction through activation of mineralcorticoid receptor

氢化可的松和甲基强的松可显著提高培养血管内皮细胞糖皮质激素的转录活性和超氧化物的产生，降低内皮型一氧化氮合酶的表达和激活。螺内酯和依普利酮可抑制上述作用。糖皮质激素过量通过激活糖皮质激素受体增强氧化应激，减弱一氧化氮的产生，导致血管内皮功能障碍。

Hydrocortisone and methylprednisolone significantly increased glucocorticoid transcriptional activity and production of superoxide, and decreased expression and activation of endothelial nitric oxide synthase in cultured vascular endothelial cells. Thease effects were suppressed by spironolactone and eplerenone. Glucocorticoid excess enhanced oxidative stress and attenuated nitric oxide production through activation of mineralcorticoid recptor, leading to vascular endothelial dysfunction.