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Furosemide blocks basolateral membrane Cl- permeability in gallbladder epithelium
J S Stoddard1, G A Altenberg, M L Ferguson
1Department of Physiology and Biophysics, University of Texas Medical Branch, Galveston 77550.
The American Journal of Physiology
|June 1, 1990
Summary
Furosemide hyperpolarizes Necturus gallbladder cells by reversibly blocking basolateral membrane chloride (Cl-) permeability. This drug affects cell membrane voltage and ion transport, impacting gallbladder function.
Area of Science:
- Physiology
- Cell Biology
- Pharmacology
Background:
- The Necturus gallbladder epithelium plays a crucial role in ion and fluid transport.
- Understanding the mechanisms of ion channel regulation is vital for comprehending epithelial function.
Purpose of the Study:
- To investigate the effects of furosemide on the electrical properties of Necturus gallbladder epithelial cells.
- To determine the specific ion conductances affected by furosemide on the basolateral membrane.
Main Methods:
- Electrophysiological measurements of basolateral membrane voltage (Vcs) in Necturus gallbladders.
- Assessment of membrane voltage responses to changes in extracellular ion concentrations ([K+], [Cl-], [HCO3-]).
- Two-point intraepithelial cable analysis to estimate basolateral membrane resistance (Rb).
Main Results:
- Furosemide induced a concentration-dependent hyperpolarization of cell membranes.
- Furosemide significantly increased basolateral membrane voltage and resistance.
- The drug reduced the depolarization response to decreased serosal [Cl-] and [HCO3-], indicating reduced Cl- conductance.
Conclusions:
- Furosemide reversibly blocks basolateral membrane electrodiffusive chloride permeability in Necturus gallbladders.
- The findings suggest furosemide primarily reduces basolateral membrane Cl- conductance (Gcl).
- A potential concomitant stimulation of basolateral membrane electrodiffusive K+ permeability by furosemide is also considered.