Endothelin Induces a Rise of Inositol 1,4,5‐Trisphosphate, Inositol 1,3,4,5‐Tetrakisphosphate Levels and of Cytosolic Ca2+ Activity in Neural Cell Lines

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Abstract
The mechanism of action of the vasoconstricting peptide endothelin was investigated in two neural cell lines. In rat glioma cells endothelin‐1 caused a biphasic rise in cytosolic Ca2+ activity. A large peak of 40 s duration was followed by another, however smaller, transient rise of comparable duration. In the absence of extracellular Ca2+ only the first peak was detected. Pretreatment with Ca2+ ionophores suppressed the Ca2+ response to endothelin. At the concentrations used the Ca2+ ionophores primarily deplete internal Ca2+ stores and prevent their refilling. Measurements of 45Ca2+ fluxes corroborate the conclusion that in the glioma cells endothelin induces firstly a release of Ca2+ from internal stores and subsequently a stimulation of Ca2+ entry. In neuronal cells (mouse neuroblastoma × rat glioma hybrid cells), endothelin caused a monophasic rise in cytosolic Ca2+ activity, most likely due to release from internal stores. In the glioma cells the concentrations of both inositol 1,4,5‐trisphosphate and inositol 1,3,4,5‐tetrakisphosphate were raised about 2.5‐fold for ca. 90 s after addition of endothelin. In the neuronal cells a shorter, smaller rise in inositololigophosphate concentrations was induced. Thus, endothelin seems to act as a neuropeptide activating phospholipase C and intracellular Ca2+.

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