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Mechanisms underlying volume regulatory decrease by Necturus gallbladder epithelium.

T J Furlong¹, K R Spring

¹Laboratory of Kidney and Electrolyte Metabolism, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Maryland 20892.

The American Journal of Physiology

|June 1, 1990

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Necturus gallbladder epithelial cells exhibit volume regulatory decrease (VRD) via basolateral K channels and bumetanide-sensitive anion channels. Organic solute absorption also triggers VRD, but through a distinct shrinkage mechanism.

Area of Science:

Cell Biology
Physiology
Epithelial Transport

Background:

Volume regulatory decrease (VRD) is a critical cellular process for maintaining cell volume homeostasis.
Epithelial cells, like those in the Necturus gallbladder, possess sophisticated mechanisms to regulate cell volume in response to osmotic stress.

Purpose of the Study:

To investigate the ion channel mechanisms underlying VRD in Necturus gallbladder epithelial cells.
To differentiate the VRD pathways activated by hypotonic stress versus organic solute absorption.

Main Methods:

Perfusion of Necturus gallbladder epithelial cells with various ionic solutions and pharmacological agents (BaCl2, phencyclidine, bumetanide, phlorizin).
Measurement of cell volume changes and membrane potential.
Utilized chloride-free and thiocyanate-based Ringer solutions to assess ion transport involvement.

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Main Results:

VRD was inhibited by basolateral BaCl2 and phencyclidine, implicating K channels.
VRD was also inhibited by basolateral bumetanide in thiocyanate Ringer, suggesting involvement of bumetanide-sensitive anion channels.
Organic solute (D-glucose) absorption induced a distinct shrinkage mechanism, inhibited by basolateral bumetanide but not BaCl2 or phencyclidine.

Conclusions:

Necturus gallbladder epithelial cells utilize basolateral K channels and bumetanide-sensitive anion channels for VRD in response to hypotonicity.
Organic solute absorption activates a separate, bumetanide-sensitive shrinkage pathway, distinct from the hypotonic VRD mechanism.