Abstract
Endothelin-1 (ET-1) produced a dose-dependent increase of intracellular Ca++ concentrations [Ca++]i characterized by an early peak phase and a delayed plateau in LAN-1 human neuroblastoma cells. The ET-1 receptor showed a rapid desensitization since a second pulse application of ET-1 did not elicit a further [Ca++]i increase. Furthermore thapsigargin, an endoplasmic reticulum Ca(++)-ATPase inhibitor, completely abolished the ET-1 induced intracellular Ca++ elevation.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Calcium / metabolism*
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Cell Line
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Dose-Response Relationship, Drug
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Endothelins / pharmacology*
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Humans
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Intracellular Fluid / drug effects*
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Intracellular Fluid / physiology
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Microscopy, Fluorescence
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Neuroblastoma
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Receptors, Cell Surface / drug effects*
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Receptors, Cell Surface / physiology
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Receptors, Endothelin
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Tumor Cells, Cultured / drug effects*
Substances
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Endothelins
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Receptors, Cell Surface
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Receptors, Endothelin
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Calcium