Wambach G, Schmülling V, Kaufmann W
Cardiology. 1985;72 Suppl 1:95-8. doi: 10.1159/000173952.
The mechanism of glucocorticoid-induced hypertension is not clarified. Recent data suggest an alteration of active electrolyte transport systems by glucocorticoids. We therefore studied the activities of the Na-K pump by measuring the Na-K-ATPase activity in erythrocyte ghosts and the ouabain-sensitive uptake of rubidium in erythrocytes of patients with Cushing's syndrome and of patients with exogenous glucocorticoid excess after treatment with fluocortolone or ACTH. Na-K-ATPase activity was significantly increased in patients with Cushing's syndrome and in patients treated with ACTH compared to the controls. Similarly, total uptake of 86Rb and the ouabain-sensitive uptake in erythrocytes were found to be above the control range both in patients with Cushing's syndrome and in patients treated with fluocortolone. There was no difference in furosemide-sensitive uptake of 86Rb. The results demonstrate an increased maximal activity of the Na-K pump in patients with glucocorticoid excess.
糖皮质激素诱导高血压的机制尚不清楚。最近的数据表明糖皮质激素会改变活性电解质转运系统。因此，我们通过测量库欣综合征患者以及接受氟可的索或促肾上腺皮质激素（ACTH）治疗后出现外源性糖皮质激素过量的患者红细胞膜中的钠钾ATP酶活性以及红细胞中哇巴因敏感的铷摄取量，来研究钠钾泵的活性。与对照组相比，库欣综合征患者以及接受ACTH治疗的患者的钠钾ATP酶活性显著增加。同样，在库欣综合征患者以及接受氟可的索治疗的患者中，红细胞中86Rb的总摄取量和哇巴因敏感摄取量均高于对照范围。86Rb对呋塞米敏感的摄取量没有差异。结果表明糖皮质激素过量患者的钠钾泵最大活性增加。
