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Stimulus-permeability coupling in rat lacrimal gland
The American Journal of Physiology
|August 11, 1980
Summary
Carbachol stimulates calcium influx in cells, leading to increased sodium and potassium permeability. This suggests a novel ion transport mechanism distinct from typical excitable tissues.
Area of Science:
- Cellular Physiology
- Ion Transport Mechanisms
- Pharmacology
Background:
- Carbachol is known to activate muscarinic receptors.
- Understanding downstream signaling pathways is crucial for cellular function.
Purpose of the Study:
- To investigate the ion permeability changes induced by carbachol in isolated cells.
- To elucidate the role of calcium in mediating these permeability changes.
Main Methods:
- Utilized radioactive isotopes (22Na, 45Ca, 86Rb) to measure ion flux.
- Employed ionophores (A23187) and pharmacological agents (EGTA, cobalt, amiloride, TTX, D 600) to probe cellular mechanisms.
Main Results:
- Carbachol stimulated influx of both 22Na and 45Ca.
- Increased cytosolic calcium initiated 22Na uptake.
- Amiloride partially inhibited 22Na uptake, while D 600 showed minor effects on both Na+ and Ca2+ uptake.
- High potassium did not abolish carbachol-induced permeability changes.
Conclusions:
- Carbachol triggers calcium influx, which subsequently alters membrane permeability to sodium and potassium.
- The identified ion permeability mechanisms are specific to each ion and differ from those in excitable tissues.