Haldy P, Müller J
Am J Physiol. 1981 Jan;240(1):E12-7. doi: 10.1152/ajpendo.1981.240.1.E12.
The role of the kidneys in the stimulation of aldosterone biosynthesis by sodium sequestration was investigated in potassium-depleted rats. After 2 wk on a potassium-deficient diet, rats were treated by subcutaneous injections of polyethylene glycol or formalin and were then kept on sucrose and water for 24 h. Either type of experimental edema markedly enhanced the conversions of tritiated deoxycorticosterone and corticosterone to aldosterone and 18-hydroxycorticosterone by incubated capsular portions of the adrenal glands and partially normalized the deranged pattern of endogenous corticosteroid output in response to serotonin. Bilateral nephrectomy completely blocked these effects of edema on the zona glomerulosa. When uremia was induced by bladder resection, with the kidneys left intact, edema still significantly stimulated aldosterone biosynthesis. Irrespective of increases in the plasma creatinine, the plasma potassium remained at uniformly low levels in all experimental groups of animals. According to these observations, experimental edema stimulates late steps of aldosterone biosynthesis in potassium-depleted rats by mediation of the kidneys, most likely through the renin-angiotensin system.
在低钾血症大鼠中研究了肾脏在通过钠潴留刺激醛固酮生物合成中的作用。在低钾饮食2周后，给大鼠皮下注射聚乙二醇或福尔马林，然后让其在蔗糖和水中维持24小时。任何一种实验性水肿均显著增强了肾上腺被膜部分将氚标记的脱氧皮质酮和皮质酮转化为醛固酮和18-羟皮质酮的能力，并部分使内源性皮质类固醇输出对5-羟色胺反应的紊乱模式正常化。双侧肾切除术完全阻断了水肿对球状带的这些作用。当通过膀胱切除诱导尿毒症且肾脏保持完整时，水肿仍能显著刺激醛固酮的生物合成。无论血浆肌酐升高情况如何，所有实验组动物的血浆钾均维持在统一的低水平。根据这些观察结果，实验性水肿通过肾脏介导，很可能是通过肾素-血管紧张素系统，刺激低钾血症大鼠醛固酮生物合成的后期步骤。
