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Interaction between cell sodium and the amiloride-sensitive sodium entry step in rabbit colon
The Journal of Membrane Biology
|March 10, 1978
Summary
Cellular sodium levels regulate the amiloride-sensitive sodium entry pathway in the colon. High intracellular sodium, caused by ouabain or amphotericin B, blocks sodium transport, while depleted sodium enhances it.
Area of Science:
- Physiology
- Cell Biology
- Renal and Epithelial Physiology
Background:
- The short-circuit current (Isc) and transepithelial conductance (Gt) of the rabbit colon are affected by ouabain and amphotericin B.
- Amiloride-sensitive sodium (Na) entry is crucial for transepithelial Na transport.
Purpose of the Study:
- To investigate the regulation of the amiloride-sensitive Na entry step in rabbit colon.
- To elucidate the role of intracellular Na concentration in modulating Na transport.
Main Methods:
- Short-circuit current (Isc) and transepithelial conductance (Gt) measurements in rabbit colon.
- Exposure of Na-depleted tissues to 140 mM Na in the presence and absence of ouabain or amphotericin B.
- Analysis of amiloride-sensitive Na entry and its dependence on intracellular Na.
Main Results:
- Ouabain abolished Isc and decreased Gt, while amphotericin B increased both.
- Amiloride-sensitive Na entry was blocked by elevated intracellular Na in the presence of ouabain or amphotericin B.
- Sudden exposure of Na-depleted tissues to 140 mM Na caused a rapid increase and subsequent decline in amiloride-sensitive Isc and Gt, indicating a negative feedback mechanism regulated by intracellular Na.
Conclusions:
- The conductance of the amiloride-sensitive Na entry step is inversely regulated by intracellular Na concentration.
- A parallel cellular compartment with a large Na capacity likely mediates negative feedback on Na entry permeability.
- This system allows for rapid initiation and steady-state achievement of active transepithelial Na transport.