KCNQ1-dependent transport in renal and gastrointestinal epithelia
| Autor: | Rexhepi Rexhepaj, Harald Völkl, Kerstin Richter, Qi Rong, Florian Lang, Volker Vallon, Uwe Gerlach, Karl Pfeifer, Florian Grahammer, Ciprian D. Sandu |
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| Rok vydání: | 2005 |
| Předmět: |
Male
Epithelial sodium channel medicine.medical_specialty endocrine system diseases Biology Kidney Kidney Function Tests Amiloride Mice Parietal Cells Gastric Internal medicine medicine Animals Secretion Anemia Macrocytic Intestinal Mucosa Mice Knockout Multidisciplinary urogenital system Reabsorption Sodium Stomach Biological Transport Epithelial Cells Hydrogen-Ion Concentration Biological Sciences Intestines Glucose medicine.anatomical_structure Endocrinology Gastric Mucosa KCNQ1 Potassium Channel Potassium Gastric acid Cotransporter Homeostasis medicine.drug |
| Zdroj: | Proceedings of the National Academy of Sciences. 102:17864-17869 |
| ISSN: | 1091-6490 0027-8424 |
| DOI: | 10.1073/pnas.0505860102 |
| Popis: | Mutations in the gene encoding for the K + channel α-subunit KCNQ1 have been associated with long QT syndrome and deafness. Besides heart and inner ear epithelial cells, KCNQ1 is expressed in a variety of epithelial cells including renal proximal tubule and gastrointestinal tract epithelial cells. At these sites, cellular K + ions exit through KCNQ1 channel complexes, which may serve to recycle K + or to maintain cell membrane potential and thus the driving force for electrogenic transepithelial transport, e.g., Na + /glucose cotransport. Employing pharmacologic inhibition and gene knockout, the present study demonstrates the importance of KCNQ1 K + channel complexes for the maintenance of the driving force for proximal tubular and intestinal Na + absorption, gastric acid secretion, and cAMP-induced jejunal Cl - secretion. In the kidney, KCNQ1 appears dispensable under basal conditions because of limited substrate delivery for electrogenic Na + reabsorption to KCNQ1-expressing mid to late proximal tubule. During conditions of increased substrate load, however, luminal KCNQ1 serves to repolarize the proximal tubule and stabilize the driving force for Na + reabsorption. In mice lacking functional KCNQ1, impaired intestinal absorption is associated with reduced serum vitamin B12 concentrations, mild macrocytic anemia, and fecal loss of Na + and K + , the latter affecting K + homeostasis. |
| Databáze: | OpenAIRE |
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