In: Business and Management

Submitted By pkgupta2003
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Reabsorption of Sodium Chloride — Lessons from the Chloride Channels


prostaglandin inhibitors, and the molecular challenge is substantial as well. The molecular delineation of the genetic defects that result in tubulopathies can lead to a better understanding of their physiology. However, the DNA sequencing of the genes that encode transporters and channels (as well as their subunits) is not a trivial matter and must be complemented by experiments determining expression patterns. The Xenopus oocytes that have been used for such studies are transfected cells rather than “real” polarized cells of the thick ascending limb of the loop of Henle surrounded by the sophisticated hypertonic environment of the renal medulla.
The complex polyuria–polydipsia syndrome described by Schlingmann et al. is attributable to the concomitant loss-of-function mutations in both
CLCNKA and CLCNKB; the syndrome results in ion selectivity, demonstrating the means whereby a renal tubular cell lets one type of ion (chloride) through the lipid membrane to the exclusion of others. It thus provides yet another example of the molecular basis of Bartter’s syndrome (see Figure).

The contributions of Roderick McKinnon and
Peter Agre to solving these two complementary problems of the resorption of renal solute and renal solvent earned them the 2003 Nobel Prize in chemistry.5 We live in a fascinating time in which clinical syndromes can be deciphered at the molecular and even the atomic level.
From the Department of Medicine and the Membrane Protein
Study Group, University of Montreal (D.G.B.); and the Department of Human Genetics and Medicine, McGill University
(T.M.F.) — both in Montreal.
1. Peters M, Jeck N, Reinalter S, et al. Clinical presentation of genetically defined patients with hypokalemic salt-losing tubulopathies. Am J Med 2002;112:183-90.

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