Activation of a K+ conductance by bradykinin and by inositol-1,4,5-trisphosphate in rat glioma cells: involvement of intracellular and extracellular Ca2+

doi:10.1016/0006-8993(90)91252-C

Brain Research

Volume 506, Issue 2, 8 January 1990, Pages 205-214

https://doi.org/10.1016/0006-8993(90)91252-C Get rights and content

Abstract

Extracellular application of bradykinin and injection of inositol-1,4,5-trisphosphate (Ins-P₃) induced a hyperpolarization in polyploid rat glioma cells. Ins-1,4,5-P₃ and Ins-2,4,5-P₃ were effective but not Ins-4,5-P₂, Ins-1,3,4,5-P₄ and Ins-1,3,4,5,6-P₅. The reversal potential of the hyperpolarizing response induced by bradykinin or by Ins-P₃ increased to a comparable degree with increasing the extracellular K⁺ concentration. Certain blockers of K⁺ channels, for example charybdotoxin (5–50 nM), Ba²⁺ (5–20 mM), 4-aminopyridine (5–10 mM) and quinidine (0.1–0.5 mM) reversibly suppressed the membrane potential response to bradykinin or to Ins-P₃; however, apamin (1 μM) andd-tubocurarine (0.5 mM) had no effect. Intracellular injection of EGTA made the glioma cells unresponsive to bradykinin. Superfision of the cells with Ca²⁺-free medium gradually and reversibly abolished the response to bradykinin, but only slightly reduced the effect of Ins-P₃. The Ca²⁺ channel blockers Co²⁺ (1–5 mM), Mn²⁺ (2–6 mM) and nifedipine (1–20 μM), but not desmethoxyverapamil (100 μM) inhibited the hyperpolarizing effect of bradykinin. The hyperpolarization induced by Ins-P₃, however, was not influenced by Mn²⁺ (1–5 mM) or by Co²⁺ (7 mM). Injection of Ca²⁺ into the glioma cells induced a hyperpolarization susceptible to Ba²⁺ and quinidine. Treatment of glioma cells with an activator or with inhibitors of protein kinase C or with pertussis toxin did not affect the response to bradykinin. Incubation of the cells with the Ca²⁺ ionophore A23187 (0.1–1 μM) made the cells unresponsive to bradykinin and, somewhat less, to Ins-P₃. At these concentrations the Ca²⁺ ionophore primarily depletes intracellular Ca²⁺ stores. In summary, bradykinin, via B₂-receptors (blocked by [Thi^5,8,d-Phe⁷]-bradykinin) activates a K⁺ conductance in glioma cells following a rise of cytosolic Ca²⁺ activity most likely due to Ins-P₃-mediated release of Ca²⁺ from internal stores. Entry of extracellular Ca²⁺ appears also to be involved in this process.

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Activation of a K+ conductance by bradykinin and by inositol-1,4,5-trisphosphate in rat glioma cells: involvement of intracellular and extracellular Ca2+

Abstract

Cell

FEBS Lett.

Trends Neurosci.

Methods Enzymol.

Exp. Cell Res.

FEBS Lett.

Biochem. Biophys. Res. Commun.

Trends Neurosci.

Cell Calcium

Brain Research

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Peptides

Neurosci. Lett.

J. Biol. Chem.

Characterization of a toxin from scorpion (Leirus quinquestriatus) venom that blocks in vitro both large (BK) K+ channels in rabbit vascular smooth muscle and intermediate (IK) conductance Ca2+-activated K+ channels in human red cells

J. Physiol. (Lond.)

Inositol trisphosphate, a novel second messenger in cellular signal transduction

Nature (Lond.)

Membrane current responses of NG108-15 mouse neuroblastoma × rat glioma hybrid cells to bradykinin

J. Physiol. (Lond.)

Inositol 1,4,5 trisphosphate and diacylglycerol mimic bradykinin effects on mouse neuroblastoma × rat glioma cells

J. Physiol. (Lond.)

Effects of quinine and apamin on the calcium-dependent potassium permeability of mammalian hepatocytes and red cells

J. Physiol. (Lond.)

Actions of inositol phosphates on Ca2+ pools in guinea-pig hepatocytes

Biochem. J.

Activation of a K⁺ conductance by bradykinin and by inositol-1,4,5-trisphosphate in rat glioma cells: involvement of intracellular and extracellular Ca²⁺

Characterization of a toxin from scorpion (Leirus quinquestriatus) venom that blocks in vitro both large (BK) K⁺ channels in rabbit vascular smooth muscle and intermediate (IK) conductance Ca²⁺-activated K⁺ channels in human red cells

Actions of inositol phosphates on Ca²⁺ pools in guinea-pig hepatocytes