Correction of Increased Sympathoadrenal Activity inBartter's Syndrome by Inhibitionof Prostaglandin Synthesis

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Abstract
Sympathetic nervous system function was studied in seven patients with Bartter's syndrome and in age-matched normal controls by measurements of basal and stimulated norepinephrine concentrations in plasma and excretion of epinephrine and norepinephrine in urine. In threeof these patients, urinary metanephrine and 3-methoxy-4-hydroxyman-delic acid were also measured and the response to indomethacin was determined. In the patients, mean plasma norepinephrine was 217 ± 48 (SEM) pg⁄ml in the supine position, 489 ± 76 pg⁄ml n i the upright position, and 614± 186pg⁄ml after compression of a handgrip for 5 min. These values were not significantly different fromthose of the controls. Urinary norepinephrine excretion in the patients with Bartter's syndrome was 130.4 ± 23.0 μg⁄day compared to 73.3 ± 11.2 μg⁄day (P < 0.01)in thecontrols. Urinary epinephrine excretion was 41.5 ±3.0 μg⁄day in the patients with Bartter’ssyndrome compared to 27.8 ± 3.4 fig⁄day (P < 0.01) in the controls. Urinary metanephrine and 3-methoxy-4-hydroxymandelic acid inthe patients with Bartter’s syndrome were normal. The administration of indomethacin (150 mg⁄day) for 4 days decreased urinary norepinephrine toward normal. Theresults suggest that peripheral sympathoad-renal activity is increased in patients with Bartter’s syndrome, probably as compensation for theincrease in vascular resistance t o norepinephrine associated with hypokalemia and presumably mediated by an increase in circulating bradykinin and vascular vasodilator prostaglandins.

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