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Updated: Jul 29, 2026
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Cytosolic Calcium Measurements in Renal Epithelial Cells by Flow Cytometry
Published on: October 28, 2014
Renal transepithelial phosphate secretion: luminal membrane voltage and Ca2+ dependence
1Department of Physiology and Neurobiology, University of Connecticut, Storrs 06269-3042.
The American Journal of Physiology
|October 1, 1994
Summary
Thapsigargin stimulates phosphate secretion in flounder kidney cells. This process is influenced by apical membrane potential and calcium, potentially involving calcium-activated potassium channels.
Area of Science:
- Renal Physiology
- Cell Biology
- Ion Transport
Background:
- Transepithelial phosphate (P(i)) secretion is crucial for renal function.
- The regulation of P(i) secretion by apical membrane potential and extracellular calcium is not fully understood.
Purpose of the Study:
- To investigate the role of apical membrane electrical potential, potassium channels, and extracellular calcium in thapsigargin-induced transepithelial P(i) secretion in flounder renal proximal tubule cells.
Main Methods:
- Primary monolayer cultures of flounder renal proximal tubule cells were used in Ussing chambers.
- Apical membrane potential was measured, and the effects of luminal ion substitutions, channel blockers, and calcium concentrations were assessed.
- Phosphate secretion and movement were quantified using radiolabeled phosphate (32P(i)).
Main Results:
- Thapsigargin significantly increased net P(i) secretion.
- Luminal potassium substitution depolarized the apical membrane and inhibited P(i) secretion, suggesting K+ channel involvement.
- Calcium channel blockers and calmodulin antagonists reduced thapsigargin-stimulated P(i) secretion.
- Increased extracellular calcium enhanced P(i) secretion.
Conclusions:
- Thapsigargin-induced transepithelial P(i) secretion is significantly influenced by apical membrane electrical polarity.
- Calcium-activated potassium channels may play a role in regulating this P(i) secretion.
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