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Epithelial Na(+) channels are regulated by flow.

L M Satlin1, S Sheng, C B Woda

  • 1Department of Pediatrics, Mount Sinai School of Medicine, New York 10029-6574, USA. lisa.satlin@mssm.edu

American Journal of Physiology. Renal Physiology
|May 16, 2001
PubMed
Summary

Fluid flow stimulates sodium (Na(+)) absorption in the kidney

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Area of Science:

  • Nephrology
  • Physiology
  • Molecular Biology

Background:

  • Sodium absorption in the renal cortical collecting duct (CCD) is crucial for maintaining fluid balance.
  • Epithelial sodium channels (ENaCs) mediate this Na(+) absorption.
  • The role of biomechanical forces, like fluid flow, in regulating ENaCs is debated.

Purpose of the Study:

  • To investigate the effect of varying intraluminal flow rates on ENaC activity and Na(+) absorption in the CCD.
  • To determine whether biomechanical forces such as hydrostatic pressure, membrane stretch, or shear stress regulate ENaCs.

Main Methods:

  • Whole-cell Na(+) currents (I(Na)) were measured in oocytes expressing mouse alpha,beta,gamma-ENaC (mENaC) under superfusate flow.
  • Net Na(+) absorption was measured in microperfused rabbit CCDs subjected to altered luminal flow rates and viscosity.

Main Results:

  • Superfusate flow reversibly stimulated I(Na) threefold in mENaC-expressing oocytes.
  • Increased luminal flow rate in rabbit CCDs resulted in a twofold increase in net Na(+) absorption.
  • Increased luminal viscosity did not affect Na(+) absorption, indicating shear stress is not the primary mediator.

Conclusions:

  • Flow-induced stimulation of ENaC activity and Na(+) absorption is likely mediated by increased hydrostatic pressure and/or membrane stretch.
  • Intraluminal flow rate represents a potential physiological regulator of channel activity in the renal CCD.

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