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Ca(2+)-dependent and Ca(2+)-permeable ion channels in aortic endothelial cells
1Department of Medicine, Emory University School of Medicine, Atlanta, Georgia.
The American Journal of Physiology
|December 1, 1992
Summary
Hypotonic stress activates bovine aortic endothelial cell (BAEC) potassium channels in two phases. A calcium-permeable channel facilitates calcium influx during the delayed phase of potassium channel activation.
Area of Science:
- Cell Physiology
- Ion Transport
Background:
- Bovine aortic endothelial cells (BAECs) possess specific ion channels.
- Osmotic stress is a critical factor influencing cellular function.
Purpose of the Study:
- To investigate the activation of ion channels in BAECs under osmotic stress.
- To elucidate the role of calcium in channel activation during hypotonic conditions.
Main Methods:
- Cell-attached and inside-out patch clamp recordings were used.
- BAECs were subjected to hypotonic conditions (220 mosmol/kg).
- Ion channel activity was monitored in response to osmotic changes and pharmacological agents.
Main Results:
- Hypotonic exposure induced a biphasic activation of 165-pS and 40-pS potassium channels.
- The initial phase of K+ channel activation was independent of external Ca2+.
- A delayed, sustained K+ channel activation phase required external Ca2+ and was modulated by gadolinium.
- A 28-pS nonselective cation channel (NSCC), permeable to Ca2+, was activated by hyperpolarization and blocked by gadolinium.
Conclusions:
- Hypotonic stress activates Ca2+-dependent K+ channels in BAECs in a biphasic manner.
- External Ca2+ influx through gadolinium-sensitive NSCCs is crucial for the delayed K+ channel activation.
- These findings reveal a novel mechanism of ion channel regulation by osmotic stress in endothelial cells.