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Potassium activity and plasma membrane potentials in epithelial cells of toad bladder
The American Journal of Physiology
|March 1, 1977
Summary
Intracellular potassium activity (aki) in toad bladder epithelium was measured. Findings suggest bound potassium and reveal how vasopressin and prostaglandin E1 influence electrolyte transport.
Area of Science:
- Physiology
- Cell Biology
- Biophysics
Background:
- Intracellular potassium activity (aki) and membrane potentials are crucial for electrolyte transport.
- Understanding these parameters in toad bladder epithelium provides insights into epithelial function.
Purpose of the Study:
- To measure intracellular potassium activity (aki), mucosal and serosal membrane potentials (mEm, sEm), short-circuit current (Isc), and transepithelial potential difference in toad bladder epithelium.
- To investigate the effects of ouabain, rotenone, ethacrynic acid, vasopressin, and prostaglandin E1 on these parameters.
Main Methods:
- Utilized a potassium-sensitive liquid ion exchanger and microelectrodes for precise measurements.
- Measured aki, mEm, sEm, Isc, and transepithelial potential difference under basal and stimulated conditions.
Main Results:
- Basal aki was 41.2 +/- 0.5 mM, indicating significant bound or sequestered intracellular potassium.
- Serosal membrane potential (sEm) was lower than the potassium equilibrium potential (Eeq) and showed no direct relation.
- Vasopressin decreased aki and increased mEm; prostaglandin E1 increased aki and sEm. Ouabain and rotenone decreased aki, while ethacrynic acid affected Isc and potentials but not aki.
Conclusions:
- A substantial portion of intracellular potassium may be bound or sequestered within subcellular organelles.
- The observed changes in aki and membrane potentials provide valuable insights into the mechanisms of transcellular electrolyte transport in toad bladder epithelium.
- Hormonal regulation by vasopressin and prostaglandin E1 significantly impacts intracellular potassium dynamics and membrane potentials, influencing epithelial transport.