Müller J
Acta Endocrinol (Copenh). 1986 May;112(1):105-13.
The effects of dietary chloride restriction - alone or combined with sodium and potassium restriction - on aldosterone biosynthesis and the renin-angiotensin system were studied in rats. Treatment with a chloride-deficient diet led to a temporary decrease in the capsular adrenal conversions of corticosterone to 18-hydroxycorticosterone and aldosterone (manifest after 2 weeks but not longer apparent after 3 weeks), which was accompanied by a progressive rise in plasma renin activity and a moderate fall in plasma potassium. Combined restriction of sodium, potassium and chloride elicited a decreased activity of the enzyme(s) involved in late steps in aldosterone biosynthesis, an elevation of plasma renin activity to excessively high levels and a substantial hypokalaemia. Chloride repletion of these rats by the addition of NH4Cl or CaCl2 to their drinking fluid stimulated aldosterone biosynthesis while lowering plasma renin activity and raising plasma potassium. According to these observations, dietary chloride deficiency is another example of an experimental situation in which a high activity of the renin-angiotensin system contrasts with an unchanged or suppressed aldosterone biosynthesis. Most likely, this divergence is at least partly due to hypokalaemia which is induced during long-term chloride deficiency by a yet unknown mechanism.
在大鼠中研究了饮食中单独限制氯化物或联合限制钠和钾对醛固酮生物合成及肾素-血管紧张素系统的影响。用缺氯饮食处理导致肾上腺皮质酮向18-羟皮质酮和醛固酮的包膜肾上腺转化率暂时降低（2周后明显，但3周后不再明显），同时伴有血浆肾素活性逐渐升高和血浆钾适度下降。联合限制钠、钾和氯化物会引起醛固酮生物合成后期步骤中相关酶活性降低，血浆肾素活性升高至极高水平以及严重低钾血症。通过在这些大鼠的饮水中添加氯化铵或氯化钙补充氯化物可刺激醛固酮生物合成，同时降低血浆肾素活性并升高血浆钾。根据这些观察结果，饮食中氯化物缺乏是肾素-血管紧张素系统高活性与醛固酮生物合成未改变或受抑制形成对比的另一个实验情况实例。很可能，这种差异至少部分归因于长期氯化物缺乏期间由未知机制诱导的低钾血症。
