Abstract
Rat astrocytoma C6 cells have been recently identified as target cells for ET-1, which stimulates inositol lipid turnover in these cells. It is shown here that binding of ET-1 to high-affinity receptors on C6 cells leads to 40-45% inhibition of isoproterenol-induced intracellular cyclic AMP accumulation, as well as to stimulation of inositol lipid turnover, both effects characterized by an absolute requirement of extracellular calcium. Moreover, ET-1, which has been generally reported to have a mitogenic effect on a variety of target cells including primary rat astrocytes, is shown here to stimulate or, alternatively, inhibit DNA synthesis in C6 cells, depending on the subclone considered.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Animals
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Aorta / metabolism
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Astrocytoma / metabolism*
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Cell Membrane / metabolism
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Colforsin / pharmacology
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Cyclic AMP / metabolism
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DNA, Neoplasm / biosynthesis
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Endothelins / chemical synthesis
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Endothelins / metabolism
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Inositol Phosphates / biosynthesis
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Isoproterenol / antagonists & inhibitors
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Isoproterenol / pharmacology
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Kinetics
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Rats
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Receptors, Cell Surface / metabolism*
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Receptors, Endothelin
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Thymidine / metabolism
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Tumor Cells, Cultured / metabolism*
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Viper Venoms / chemical synthesis
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Viper Venoms / metabolism
Substances
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DNA, Neoplasm
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Endothelins
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Inositol Phosphates
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Receptors, Cell Surface
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Receptors, Endothelin
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Viper Venoms
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sarafotoxins s6
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Colforsin
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Cyclic AMP
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Isoproterenol
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Thymidine