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Direct evidence for apical Na+:2Cl-:K+ cotransport in macula densa cells
J Y Lapointe1, P D Bell, J Cardinal
1Membrane Transport Research Group, University of Montreal, Quebec, Canada.
The American Journal of Physiology
|May 1, 1990
Summary
This study identifies the apical Na+:2Cl-:K+ transporter in macula densa cells, crucial for regulating salt transport in the kidneys. This transporter
Area of Science:
- Nephrology
- Renal Physiology
- Molecular Biology
Background:
- Macula densa (MD) cells play a key role in regulating glomerular filtration rate.
- The mechanism of apical sodium chloride (NaCl) transport in MD cells was previously unidentified.
Purpose of the Study:
- To determine the specific pathway for apical NaCl transport in macula densa cells.
- To elucidate the role of ion transporters in MD cell response to varying NaCl concentrations.
Main Methods:
- Utilized microdissected cortical thick ascending limbs (CTAL) with attached glomeruli.
- Employed conventional microelectrode techniques to measure basolateral membrane voltage (Vbl).
- Manipulated luminal NaCl, Na+, Cl-, and K+ concentrations.
Main Results:
- Furosemide blocked NaCl-induced repolarization, indicating its involvement in apical transport.
- Low luminal NaCl concentrations reversed the direction of NaCl transport, causing depolarization.
- Increased luminal Na+ or Cl- individually depolarized Vbl, suggesting both ions are critical.
- Removal of luminal K+ hyperpolarized Vbl, consistent with a K+-dependent transporter.
Conclusions:
- Results strongly support the presence of an apical Na+:2Cl-:K+ transporter in MD cells.
- This transporter facilitates NaCl reabsorption at high luminal NaCl concentrations.
- The transporter mediates NaCl secretion at low luminal NaCl concentrations, indicating a dual role in renal salt handling.