Activation of bradykinin B2 receptors increases calcium entry and intracellular mobilization in C9 liver cells.

J A García-Sáinz, S E Avendaño-Vázquez
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引用次数: 2

Abstract

In C9 rat liver cells bradykinin and kallidin increased (approximately 2-fold) the intracellular concentration of calcium, but the B1 agonist, des-Arg9-bradykinin did not. The effect of bradykinin was inhibited by the B2 antagonists, Hoe 140 and N-alpha-adamantaneacetyl-D-Arg-[Hyp3, Thi5,8, D-Phe7]-bradykinin, but not by the B1 antagonist, des-Arg9-[Leu8]-bradykinin. The action of bradykinin was diminished, but not abolished, in medium without calcium. The peptide was able to increase intracellular calcium concentration in cells treated with thapsigargin. Bradykinin action was not observed in cells previously stimulated with this local mediator: however, under the same conditions, angiotensin II induced a clear increase in intracellular calcium concentration. Our data indicate that activation of bradykinin B2 receptors increase intracellular calcium concentrations by inducing both gating of the cation and intracellular mobilization in C9 liver cells. In addition, homologous desensitization was observed.

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缓激素B2受体的激活增加C9肝细胞的钙进入和细胞内动员。
在C9大鼠肝细胞中,缓激肽和钾碱增加(约2倍)细胞内钙浓度,但B1激动剂des- arg9 -缓激肽没有。B2拮抗剂ho140和n - α -金刚烷乙基- d -精氨酸-[Hyp3, Thi5,8, D-Phe7]-缓激肽能抑制缓激肽的作用,而B1拮抗剂des-Arg9-[Leu8]-缓激肽不能抑制缓激肽的作用。在不含钙的培养基中,缓激肽的作用减弱,但未完全消除。该肽能够增加细胞内钙浓度处理的细胞与thapsigargin。在先前用这种局部介质刺激的细胞中未观察到缓激素的作用:然而,在相同的条件下,血管紧张素II诱导细胞内钙浓度明显增加。我们的数据表明,缓激肽B2受体的激活通过诱导C9肝细胞的阳离子门控和细胞内动员来增加细胞内钙浓度。此外,还观察到同源脱敏。
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