Initial potassium loss and hypokalaemia during chlorthalidone administration in patients with essential hypertension: the influence of dietary sodium restriction
Initial potassium loss and hypokalaemia during chlorthalidone administration in patients with essential hypertension: the influence of dietary sodium restriction
复制标题
原发性高血压患者服用氯噻酮期间的初始钾丢失和低钾血症：饮食限制钠的影响
DOI：
10.1111/j.1365-2362.1978.tb00829.x
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发表时间：
1978
影响因子：
5.5
通讯作者：
A. Struwenberg
中科院分区：
文献类型：
--
作者：
R. Landmann;A. Struwenberg
抽象的。为了研究口服利尿剂给药期间的初始钾丢失和低钾血症的发生，对10例既往口服利尿剂治疗后出现低钾血症的原发性高血压患者进行了代谢平衡研究。给予氯噻酮（每日50 mg）14天。6例患者接受正常钠饮食，4例患者接受低钠（17 mmol/天）饮食。所有患者的初始全身钾含量均正常（40 K）。测量电解质平衡、体重、溴化物空间、血浆肾素活性和醛固酮分泌率。在这两个组钾赤字的发展，与比例较大的损失，从细胞外比从细胞内室。在正常钠组中，第9天的最高平均钾缺乏为176 mmol，之后恢复了一些钾;在低钠组中，第13天的最高钾缺乏为276 mmol。正常钠组显示肾素和醛固酮水平立即但暂时的升高;低钠组的肾素和醛固酮升高较慢，但仍保持升高。可以得出结论，饮食钠限制增加利尿剂诱导的钾丢失，可能是由于肾素-血管紧张素-醛固酮系统的活性增加，而向远端肾小管的钠输送仍然足够高，以增加钾分泌。
Abstract. To investigate the initial potassium loss and development of hypokalaemia during the administration of an oral diuretic, metabolic balance studies were performed in ten patients with essential hypertension who had shown hypokalaemia under prior oral diuretic treatment. Chlorthalidone (50 mg daily) was given for 14 days. Six patients received a normal‐sodium diet and four a low‐sodium (17 mmol/day) diet. All patients had a normal initial total body potassium (40K). The electrolyte balances, weight, bromide space, plasma renin activity, and aldosterone secretion rate were measured. In both groups a potassium deficit developed, with proportionally larger losses from the extracellular than from the intracellular compartment. In the normal‐sodium group the highest mean potassium deficit was 176 mmol on day 9, after which some potassium was regained; in the low‐sodium group the highest deficit was 276 mmol on day 13. The normal‐sodium group showed an immediate but temporary rise of the renin and aldosterone levels; in the low‐sodium group renin and aldosterone increased more slowly but remained elevated. It is concluded that dietary sodium restriction increases diuretic‐induced potassium loss, presumably by an increased activity of the renin‐angiotensin‐aldo‐sterone system, while sodium delivery to the distal renal tubules remains sufficiently high to allow increased potassium secretion.