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