Effect of indomethacin in a patient with Bartter's syndrome: evidence against a primary role of prostaglandin in this disorder.

It has been claimed that in patients with Bartter's syndrome, enhanced prostaglandin synthesis causes the blunted vasopressor response to angiotensin II. The present study was undertaken to test this hypothesis by administering indomethacin to a patient with Bartter's syndrome. In domethacin corrected the subnormal pressor response to angiotensin II and lowered plasma renin activity from 115 to 15 ng/ml/hr. This effect was associated with renal sodium retention and a 7% increase in body weight. In contrast, when indomethacin was given but the sodium retention prevented by concomitant administration of furosemide, the blunted vasopressor response to angiotensin II and the hyperreninemia were not corrected. It is concluded that the effectiveness of indomethacin to correct the hyperreninemia and the blunted vasopressor to angiotensin II in the preset patient was due in large part to the ability of the drug to correct sodium balance rather than by inhibition of prostaglandin synthesis.