Abstract
To the Editor: A consistent finding in patients with Bartter's syndrome is a reduction in the ex vivo responsiveness of their platelets to such aggregating agents as adenosine diphosphate (ADP), epinephrine, thrombin, and collagen.1 2 3 This platelet defect is probably due to a circulating plasma factor, since the defect can be readily conferred on normal platelets by suspending them in plasma obtained from a subject with Bartter's syndrome.1 2 3 That this factor is a prostacyclin-like compound is suggested by the observations that the platelet defect can be alleviated both by inhibition of prostaglandin synthesis1 2 3 and by antibodies against prostacyclin.3 However, unlike prostacyclin, . . .