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Urinary excretion of 2, 3 dinor-6-keto-PGF1 alpha, a metabolite of prostacyclin (PGI2), was measured in 9 patients with Bartter's syndrome. The rate of excretion of this metabolite was normal in these patients during ingestion of both a normal and high dietary intake of potassium. This suggests that in Bartter's syndrome the rate of entry of PGI2 into the circulation is normal. Excessive systemic synthesis of PGI2 is therefore unlikely to be an explanation for either the vascular insensitivity to angiotensin II or the defect in platelet aggregation characteristic of the syndrome.