Captopril and Bartter’s Syndrome

Haruka Sasaki, MD, First Department of Internal Medicine, Fukuoka University, School of Medicine, Nanakuma, Fukuoka 814-01 (Japan) Dear Sir, We read the letters by Heneet al. [1] and by Aurellet al. [2] on the effect of captopril in Bartter’s syndrome (BS) with great interest. The clinical features and therapeutic focus in BS are chronic hypotension and severe hypokal-emia, but the ideal therapy for patients with BS remains to be determined. Captopril is an oral angiotensin-con-verting enzyme (kininase II) inhibitor and blocks the formation of angiotensin II, resulting in the reduction of aldosterone secretion [3]. As hypokalemia in BS is in part due to the hyperactivity of the renin-antiotensin-aldoste-rone system, the use of captopril may have to be considered. However, it is generally accepted that renal potassium loss is not solely due to hyperaldosteronism, because bilateral adrenalectomy fails to relieve severe hypokalemia [4]. Furthermore, even when aldosterone is suppressed to the normal range by drugs such as aminog-lutethimide, dexamethasone and prostaglandin (PG) synthesis inhibitors, serum potassium levels remain low [5,6]. In addition, aldosterone secretion may be normal or even reduced in some patients with BS [7,11]. We treated 2 patients with BS [1 was previously reported in detail by Sasakiet al., 5] in whom the initial dose of captopril (12.5 mg, p.o.) induced severe hypotension within 30–60 min and in whom exogenous angiotensin II and/or norepinephrine infusion was required constantly for at least 7 h to maintain even ordinary blood pressure levels. One of these patients received a PG synthesis inhibitor, indomethacin, rectally during the vasoconstrictor infusion. PG synthesis inhibitors do not only enhance the pressor response to injected vasoconstrictors but also attenuate the hypotensive effects of captopril (fig. 1). In another patient, unexplained tetany occurred within 60 min after captopril administration. We reported that an angiotensin II antagonist (1Sar,8-Ile AII) led to high circulating levels of angiotensin II in this syndrome (even furosemide abuse with BS) contributes to blood pressure maintenance [8, 9]. However, we did not expect captopril to induce such a severe fall in blood pressure. Although the effects of captopril on PG production are inconclusive, the involvement of PG in these effects may be hypothesized by virtue of the fact that kinins are potent stimulators of PG synthesis and release