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Aldosterone induces rapid apical translocation of ENaC in early portion of renal collecting system: possible role of SGK

  • Loffing, Johannes Institute of Anatomy, University of Zürich, CH-8057 Zürich;
  • Zecevic, Marija Institute of Physiology and
  • Féraille, Eric Division de Néphrologie, Hôpital Cantonal Universitaire, CH-1211 Geneva;
  • Kaissling, Brigitte Institute of Anatomy, University of Zürich, CH-8057 Zürich;
  • Asher, Carol Department of Biological Chemistry, The Weizmann Institute of Science, Rehovot, Israel;
  • Rossier, Bernard C. Institut de Pharmacologie et de Toxicologie, Université de Lausanne, CH-1005 Lausanne, Switzerland;
  • Firestone, Gary L. Department of Molecular and Cell Biology and The Cancer Research Laboratory, University of Califonia, Berkeley 94720; and
  • Pearce, David Division of Nephrology, Department of Medicine and Cellular and Molecular Pharmacology, University of California San Francisco, San Francisco, California 94143
  • Verrey, François Institute of Physiology and
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Published in:
  • American Journal of Physiology-Renal Physiology. - American Physiological Society. - 2001, vol. 280, no. 4, p. F675-F682
Urology
Physiology
English Aldosterone controls sodium reabsorption and potassium secretion in the aldosterone-sensitive distal nephron (ASDN). Although clearance measurements have shown that aldosterone induces these transports within 30–60 min, no early effects have been demonstrated in vivo at the level of the apical epithelial sodium channel (ENaC), the main effector of this regulation. Here we show by real-time RT-PCR and immunofluorescence that an aldosterone injection in adrenalectomized rats induces α-ENaC subunit expression along the entire ASDN within 2 h, whereas β- and γ-ENaC are constitutively expressed. In the proximal ASDN portions only, ENaC is shifted toward the apical cellular pole and the apical plasma membrane within 2 and 4 h, respectively. To address the question of whether the early aldosterone-induced serum and glucocorticoid-regulated kinase (SGK) might mediate this apical shift of ENaC, we analyzed SGK induction in vivo. Two hours after aldosterone, SGK was highly induced in all segment-specific cells of the ASDN, and its level decreased thereafter. In Xenopus laevis oocytes, SGK induced ENaC activation and surface expression by a kinase activity-dependent mechanism. In conclusion, the rapid in vivo accumulation of SGK and α-ENaC after aldosterone injection takes place along the entire ASDN, whereas the translocation of α,β,γ-ENaC to the apical plasma membrane is restricted to its proximal portions. Results from oocyte experiments suggest the hypothesis that a localized activation of SGK may play a role in the mediation of ENaC translocation.
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  • English
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green
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https://sonar.rero.ch/global/documents/1625
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