Müller J, Hofstetter L, Schwendener-Canlas P, Brunner D B, Lund E G
Endocrinology. 1984 Jul;115(1):350-6. doi: 10.1210/endo-115-1-350.
The role of the renin-angiotensin system in the adaptation of late steps in aldosterone biosynthesis to sodium intake was studied in potassium-deficient rats. Capsular portions of adrenal glands were incubated with [3H]corticosterone and conversion to aldosterone and 18-hydroxycorticosterone was measured by double isotope dilution and multiple paper chromatography. Sodium loading of sodium- and potassium-depleted rats resulted in a rapid and extensive fall in PRA but only in a delayed and gradual suppression of aldosterone biosynthesis. Treatment with the converting enzyme inhibitor, captopril, did not affect aldosterone biosynthesis in rats with established sodium and potassium deficiency, but blocked the stimulation of the conversion of corticosterone to aldosterone and 18-hydroxycorticosterone by sodium restriction of potassium-depleted rats. Infusion of a high dose of angiotensin II into potassium-deficient rats stimulated aldosterone biosynthesis depending upon the concurrent sodium intake. Accordingly, the renin-angiotensin system plays an important but limited role in the control of late steps of aldosterone biosynthesis by sodium intake. Angiotensin II seems to be essential for the induction but not for the maintenance of a high activity of the enzyme(s) involved in the conversion of corticosterone to aldosterone during combined sodium and potassium restriction. The sensitivity of the zona glomerulosa to the long term stimulatory action of angiotensin II varies with the sodium intake and appears to be regulated by the plasma potassium concentration and unknown other mediators.
在低钾大鼠中研究了肾素 - 血管紧张素系统在醛固酮生物合成后期步骤对钠摄入的适应性中的作用。将肾上腺的被膜部分与[3H]皮质酮一起孵育，并通过双同位素稀释和多次纸色谱法测量其向醛固酮和18 - 羟皮质酮的转化。钠和钾缺乏的大鼠进行钠负荷后，血浆肾素活性（PRA）迅速且大幅下降，但醛固酮生物合成仅延迟且逐渐受到抑制。用转化酶抑制剂卡托普利治疗，对已确定存在钠和钾缺乏的大鼠的醛固酮生物合成没有影响，但可阻断低钾大鼠因钠限制而对皮质酮向醛固酮和18 - 羟皮质酮转化的刺激作用。向低钾大鼠输注高剂量的血管紧张素II可刺激醛固酮生物合成，这取决于同时的钠摄入量。因此，肾素 - 血管紧张素系统在通过钠摄入控制醛固酮生物合成后期步骤中起重要但有限的作用。在钠和钾联合限制期间，血管紧张素II似乎对诱导参与皮质酮转化为醛固酮的酶的高活性是必需的，但对维持该活性并非必需。球状带对血管紧张素II长期刺激作用的敏感性随钠摄入量而变化，并且似乎受血浆钾浓度和其他未知介质调节。
