Aurell M, Rudin A
Nephron. 1983;33(4):274-8. doi: 10.1159/000182968.
3 patients with Bartter's syndrome were studied under metabolic ward conditions before and during administration of captopril 25 mg t.i.d. The drug induced an immediate and sustained reduction of blood pressure (by 14 and 18% after 1 h and 3 days, respectively) with no change in heart rate. During treatment renal plasma flow increased by 29%, but the glomerular filtration rate was unchanged. Renal vascular resistance decreased by 41%. There was an increase in urinary sodium excretion with a corresponding reduction of body weight. The potassium balance was not affected. The concentration of angiotensin II became normal but the plasma renin concentration rose tenfold. Plasma renin substrate, initially rather low, was further reduced. The blood pressure responsiveness to angiotensin II increased without being completely normalized. An abnormal production of vasodilating prostaglandins is thought to be an important feature of Bartter's syndrome. Our findings, notably the marked renal vasodilatation, may reflect the effect of these prostaglandins when unopposed by an increased angiotensin II production.
对3例巴特综合征患者在代谢病房条件下进行研究，观察服用卡托普利25毫克每日3次之前及期间的情况。该药物使血压立即且持续降低（1小时和3天后分别降低14%和18%），心率无变化。治疗期间肾血浆流量增加29%，但肾小球滤过率未变。肾血管阻力降低41%。尿钠排泄增加，体重相应减轻。钾平衡未受影响。血管紧张素II浓度恢复正常，但血浆肾素浓度升高至原来的10倍。血浆肾素底物最初较低，进一步降低。血压对血管紧张素II的反应性增加，但未完全恢复正常。血管舒张性前列腺素的异常产生被认为是巴特综合征的一个重要特征。我们的发现，尤其是明显的肾血管舒张，可能反映了这些前列腺素在未被增加的血管紧张素II产生所对抗时的作用。
