Altered membrane sodium transport in Bartter's syndrome

Correction of hypokalemia corrects the abnormalities in erythrocyte sodium transport in Bartter's syndrome.

“…However, subsequent investigators have consistently found the opposite, although only Oliver et al (6) reported this difference to be statistically significant. The different findings of Gardner et al (5) may result from an unusually high total sodium efflux rate constant in their control group. Oliver et al (6) in a study of one family with five affected siblings, five unaffected siblings, and their unaffected parents further fractionated Na+ efflux into pump (ouabain-sensitive) and nonpump (ouabainresistant) rate constants.…”

“…Several groups of investigators have used erythrocytes as potential tools with which to investigate these membrane transport processes in patients with Bartter's syndrome (5-9). In 1972, Gardner et al (5) found that the rate constant for total sodium efflux was lower in 6 out of 8 patients with Bartter's syndrome than in a group of 16 normal subjects. However, subsequent investigators have consistently found the opposite, although only Oliver et al (6) reported this difference to be statistically significant.…”

“…Several groups of investigators, postulating that a transport defect in the kidney tubule in Bartter's syndrome may result from a generalized membrane defect, have studied sodium transport in erythrocyte from these patients (5)(6)(7)(8)(9). They uniformly found that erythrocytes from patients with Bartter's syndrome contained an elevated intracellular sodium concentration.…”

“…by Beilin et al (12), by centrifuging the samples in special tubes with an internal diameter of their lower half of 5 mm at 17,000 g for 5 min. The amount of trapped Na' was estimated to be 4.8% of the buffer Na' concentration.…”

Potential therapeutic applications of aspirin and other cyclo‐oxygenase inhibitors.

“…These patients did not suffer from thirst or hypertension, and the administration of spirinolactone or potassium salts produced only a slight improvement in the hypokalaemia. The familial nature of this condition has been suggested and Bartter, Gill & Frolich (1977) and Gardner, Simopoulos, Lapey & Shibolet (1972) have noted elevated sodium and reduced potassium concentration in striated muscle biopsies and red blood cells obtained from cases of this syndrome. This suggested to Bartter et al that the main defect was one of electrolyte transport in the blood vessels, which then produced the changes in renin and aldosterone output.…”