Summary
Addition of the nonapeptide bradykinin to human A431 epidermoid carcinoma cells causes an immediate release of inositol phosphates and a rapid rise in [Ca2+]i. Half-maximal stimulation occurs at a bradykinin concentration of 4 nM. In the continuous presence of a saturating hormone concentration (1 μM) the inositol phosphate accumulation levels off within approximately 2 min; however, subsequent stimulation with histamine, another activator of phospholipase C, gives an additional increase in inositol phosphate production. Separation of the inositol phosphates by HPLC-anion exchange chromatography, reveals a rapid but transient accumulation of Ins(1,4,5)P3, followed by an increase in Ins (1,3,4,5)P4 and Ins(1,3,4)P3. Our data support a precursor/product-relationship between Ins(1,4,5)P3 and Ins(1,3,4)P3 with Ins(1,3,4,5)P4 as intermediate and argue against a messenger role of Ins(1,3,4,5)P4 and Ins(1,3,4)P3 in Ca2+ signalling.
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Tilly, B.C., van Paridon, P.A., Verlaan, I., Wirtz, K.W.A., de Laat, S.W., Moolenaar, W.H. (1987). Bradykinin-Induced Inositol Phosphate Metabolism in Human A431 Epidermoid Carcinoma Cells. In: Wirtz, K.W.A. (eds) Membrane Receptors, Dynamics, and Energetics. NATO ASI Series, vol 133. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5335-5_3
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DOI: https://doi.org/10.1007/978-1-4684-5335-5_3
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