PROSTACYCLIN OVERPRODUCTION IN BARTTER'S SYNDROME

Urinary excretion of 6-keto-prostaglandin F₁α and thromboxane B₂, the major metabolites of prostacyclin and of thromboxane A₂, respectively, was measured by specific radioimmunoassays in five female patients with Bartter's syndrome and in five normal female controls. The patients with Bartter's syndrome excreted about four times as much 6-keto-PGF₁α as the controls; their excretion of thromboxane B₂ was no different from that of the controls. These data suggest that overproduction of prostacyclin mediates both the hyper-reninæmia and the hyporesponsiveness of blood-pressure to pressor agents in Bartter's syndrome.