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*
Division of Nephrology and Endocrinology, University of Tokyo, Tokyo,
Japan
Department of Biological Sciences, Tokyo Institute of Technology,
Yokohama, Japan
Division of Nephrology and Hypertension, Georgetown University Medical
Center, Washington, DC.
Correspondence to Dr. Akihiro Tojo, Division of Nephrology and Endocrinology, Department of Internal Medicine, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Phone: +81-3-3815-5411, ext. 33056; Fax: +81-3-3814-0021; E-mail: tojyo-2im{at}h.u-tokyo.ac.jp
Abstract. Inward rectifier potassium channels (Kir) play an important role in the K+ secretion from the kidney. Recently, a new subfamily of Kir, Kir7.1, has been cloned and shown to be present in the kidney as well as in the brain, choroid plexus, thyroid, and intestine. Its cellular and subcellular localization was examined along the renal tubule. Western blot from the kidney cortex showed a single band for Kir7.1 at 52 kD, which was also observed in microdissected segments from the thick ascending limb of Henle, distal convoluted tubule (DCT), connecting tubule, and cortical and medullary collecting ducts. Kir7.1 immunoreactivity was detected predominantly in the DCT, connecting tubule, and cortical collecting duct, with lesser expression in the thick ascending limb of Henle and in the medullary collecting duct. Kir7.1 was detected by electron microscopic immunocytochemistry on the basolateral membrane of the DCT and the principal cells of cortical collecting duct, but neither type A nor type B intercalated cells were stained. The message levels and immunoreactivity were decreased under low-K diet and reversed by low-K diet supplemented with 4% KCl. By the double-labeling immunogold method, both Kir7.1 and Na+, K+-ATPase were independently located on the basolateral membrane. In conclusion, the novel Kir7.1 potassium channel is located predominantly in the basolateral membrane of the distal nephron and collecting duct where it could function together with Na+, K+-ATPase and contribute to cell ion homeostasis and tubular K+ secretion.
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