López J M, Arteaga E, Rodriguez J A, Croxatto H
Clin Sci (Lond). 1983 Nov;65(5):487-90. doi: 10.1042/cs0650487.
The effect of dexamethasone administration for 3 days on urinary kallikrein excretion was studied in 12 normal men with normal sodium intake (n = 6) or low sodium intake (n = 6). Urinary excretion of sodium, potassium, 17-hydroxycorticosteroids, aldosterone and water was also measured in all subjects. Dexamethasone administration was associated with a significant increase in urinary kallikrein excretion (F3, 30 = 6.9; P less than 0.001) regardless of sodium intake. No significant correlation could be established between the increase in urinary kallikrein excretion and changes in urinary sodium, potassium, 17-hydroxycorticosteroids, aldosterone or water. These results suggest that dexamethasone can exert a direct action on the renal kallikrein-kinin system.
在12名钠摄入量正常(n = 6)或低钠摄入量(n = 6)的正常男性中,研究了连续3天给予地塞米松对尿激肽释放酶排泄的影响。同时还测量了所有受试者尿钠、钾、17 - 羟皮质类固醇、醛固酮和水的排泄量。无论钠摄入量如何,给予地塞米松均与尿激肽释放酶排泄量显著增加相关(F3, 30 = 6.9;P < 0.001)。尿激肽释放酶排泄量的增加与尿钠、钾、17 - 羟皮质类固醇、醛固酮或水的变化之间未发现显著相关性。这些结果表明,地塞米松可对肾脏激肽释放酶 - 激肽系统产生直接作用。