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(Hypertension. 1997;30:1338-1341.)
© 1997 American Heart Association, Inc.

Articles

Membrane Ion Transport in Bartter's Syndrome

Evidence for a New Syndrome Subtype

Wladimir Koren; Edna Peleg; Talma Rosenthal; ; Yuvenaly V. Postnov

From the Chorley Institute for Hypertension, Sheba Medical Center Tel Hashomer and Sackler Faculty of Medicine, Tel Aviv University (Israel) (W.K., E.P., T.R.), and the Department of Pathology, The Cardiology Center, Moscow, Russia (Y.V.P.).

Abstract Fifteen patients with Bartter's syndrome (hyponatremic hypochloremic hypokalemic metabolic alkalosis) were compared with 15 healthy volunteers. Red blood cell Na⁺/H⁺ and Cl^-/HCO₃^- exchanges were enhanced in all patients with Bartter's syndrome. In calciuric normomagnesemic patients, sensitive to nonsteroidal anti-inflammatory drugs (classic Bartter's syndrome), red blood cell Na⁺,K⁺,2Cl^- cotransport was markedly reduced, calcium-dependent K⁺ permeability was moderately increased, and up to 60% of sodium permeability was represented by cAMP-activated fraction (presumably human analog of ß-isoform of Na⁺/H⁺ exchange). In noncalciuric hypomagnesemic patients insensitive to indomethacin (Gitelman's syndrome), Na⁺,K⁺,2Cl^- cotransport was enhanced, Na⁺ permeability was increased due to calmodulin-dependent fraction, and calcium-dependent K⁺ permeability was markedly enhanced. A new subtype of Bartter-like syndrome ("variant Bartter's syndrome") has been described in which calciuria, hypomagnesemia, and insensitivity to nonsteroidal anti-inflammatory drugs were associated with decreased Na⁺,K⁺,2Cl^- cotransport, enhanced calmodulin-activated fraction of Na⁺ influx, and reduced calcium-dependent K⁺ permeability.

Key Words: Na⁺-H⁺ exchanger • Na⁺,K⁺,2Cl^- cotransport • Cl^-/HCO₃^- exchange • calcium-dependent potassium channels • Bartter's syndrome • erythrocytes

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