Effect of Sodium Restriction and Angiotensin II Infusion in Bartter's Syndrome

Extract: Five patients with Bartter's syndrome were investigated. Sodium restriction (<10 mEq/day for at least 5 days) showed a renal sodium wastage in only two patients (I and II) in spite of increased aldosterone secretion rate (from 151–427 to 680–842 µg/day). The effect of angiotensin II (A II) 80 ng/kg/min for 30–180 min, on plasma renin activity (PRA), plasma aldosterone, and urinary sodium excretion was compared with the effect of a previous infusion of 5% dextrose given at the same rate, 0.5 ml/min for 1 hr. A II infusion resulted in increased plasma aldosterone levels: from 236–330 pg/ml to 800–881 pg/ml in 30 min. This increase was also observed in patient II (from 139 to 600 pg/ml). PRA was decreased by A II infusion (from 1,142–2,462 to 121–1,625 ng/liter/min). In patient IV, this decrease in PRA was also observed when he was on a salt-restricted diet (from 1,934 to 370 ng/liter/min); but the minimal PRA was still higher (370 ng/liter/min) than with a normal diet (121 ng/liter/min). In no case could normal PRA level be obtained. A II infusion induced an increase in urinary sodium excretion only in the two patients with renal sodium wastage (from 80–90 to 265–230 µEq/min in 30 min). Urinary sodium excretion decreased in the other patients from (37.5–213 to 4.30–46 µEq/min) and fractional sodium excretion was reduced in patient V (from 0.56% to 0.45% at 30 min and to 0.29% at 120 min). No significant change with A II infusion was observed in patient IV when he was on a sodium-restricted diet (from 1 to 2.5 µEq/min in 30 min). Urinary potassium excretion was similar to sodium excretion. No change was observed in plasma potassium and sodium.Speculation: Hypersecretion of renin is not autonomous in Bartter's syndrome. It is not explained by an insensitive feedback effect of A II on renin secretion. Hypokalemia contributes to this high level of PRA. Salt craving, which is found in 50% of the cases (ZS), is increased by A II. Nevertheless, the presence of renal sodium wastage cannot be explained only by the high A II levels which are constant in this syndrome. A deficient Na-K-ATPase activity is postulated in such cases.