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Cytosolic [Ca2+] signaling pathway in macula densa cells
1Nephrology Research and Training Center, Division of Nephrology, Departments of Medicine and Physiology, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
The American Journal of Physiology
|September 14, 1999
Summary
Macula densa cells detect sodium chloride levels via calcium signaling. Increased luminal sodium chloride raises cytosolic calcium, involving specific transporters and channels.
Area of Science:
- Nephrology
- Cell Physiology
- Renal Physiology
Background:
- Macula densa (MD) cells are crucial for regulating kidney function.
- Previous studies suggested MD cells sense luminal sodium chloride ([NaCl]l) via cytosolic calcium ([Ca2+]c) changes.
Purpose of the Study:
- To investigate the mechanism by which macula densa cells detect variations in luminal sodium chloride concentration.
- To elucidate the role of cytosolic calcium in this detection process.
Main Methods:
- Utilized fluorescence microscopy with fura 2 to measure cytosolic calcium in isolated perfused rabbit kidney tubules.
- Varied luminal [NaCl]l and observed effects on [Ca2+]c.
- Tested the impact of furosemide, nifedipine, and NPPB on [Ca2+]c responses.
Main Results:
- Increasing luminal [NaCl]l from 25 mM to 150 mM significantly elevated MD [Ca2+]c by 39.1 nM.
- This calcium increase was concentration-dependent between 0 and 60 mM [NaCl]l.
- Luminal furosemide, basolateral nifedipine, and NPPB abolished the [NaCl]l-induced [Ca2+]c rise, while BAY K 8644 increased [Ca2+]c.
Conclusions:
- Macula densa cells detect luminal sodium chloride variations through a signaling pathway.
- This pathway involves Na+-2Cl--K+ cotransport, basolateral depolarization via Cl- channels, and voltage-gated calcium channel activation.