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Updated: Feb 23, 2026

Culturing Primary Rat Inner Medullary Collecting Duct Cells
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Uninephrectomy and apical fluid shear stress decrease ENaC abundance in collecting duct principal cells.

T Ernandez1,2, K Udwan2, A Chassot2

  • 1Service of Nephrology, University Hospital of Geneva , Geneva , Switzerland.

American Journal of Physiology. Renal Physiology
|September 8, 2017
PubMed
Summary
This summary is machine-generated.

Unilateral nephrectomy downregulates the gamma epithelial sodium channel (ENaC) subunit in mice kidneys. Fluid shear stress in collecting duct cells also reduces beta and gamma ENaC subunits, impacting sodium reabsorption.

Keywords:
epithelial sodium channelshear stresssodium reabsorptionuninephrectomyvolume homeostasis

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Area of Science:

  • Nephrology
  • Molecular Biology
  • Physiology

Background:

  • Acute nephron reduction, such as after kidney donation, can elevate hypertension risk.
  • Uninephrectomy causes significant hemodynamic shifts in the remaining kidney, increasing single-nephron GFR and distal nephron fluid delivery.
  • Previous studies indicate reduced sodium fractional reabsorption post-uninephrectomy in animals maintaining volume homeostasis.

Purpose of the Study:

  • To investigate the impact of unilateral nephrectomy on epithelial sodium channel (ENaC) subunit expression in mice.
  • To explore the role of fluid shear stress (FSS) in regulating sodium reabsorption after nephron reduction.

Main Methods:

  • Mice underwent unilateral nephrectomy to assess changes in ENaC subunit expression.
  • In vitro studies applied fluid shear stress to collecting duct principal cells to examine ENaC regulation.
  • Analysis included surface expression, transcriptional levels, and involvement of signaling pathways like protein kinase A and phospholipase A2.

Main Results:

  • Unilateral nephrectomy specifically downregulated the gamma-ENaC subunit surface expression.
  • Aldosterone-sensitive alpha-ENaC and alpha1-Na-K-ATPase, along with kidney-specific cotransporters, remained unchanged.
  • In vitro, fluid shear stress downregulated beta- and gamma-ENaC subunits transcriptionally via an unidentified paracrine factor, involving PKA and calcium-sensitive cPLA2, but not primary cilia.

Conclusions:

  • Unilateral nephrectomy induces specific downregulation of gamma-ENaC, suggesting a role in altered sodium handling.
  • Fluid shear stress emerges as a key regulator of ENaC expression in collecting ducts, impacting sodium reabsorption post-nephrectomy.
  • The findings highlight novel mechanisms in kidney adaptation to nephron loss, potentially relevant to hypertension development.