Fu T, Gu Z L, Xu Y H
Laboratory of Cellular and Molecular Oncology, Shanghai Institute of Cell Biology, Chinese Academy of Sciences.
Zhongguo Yao Li Xue Bao. 1994 Nov;15(6):511-5.
Modulation of bradykinin (BK)-induced intracellular Ca2+ oscillations was investigated with single cell Ca2+ analysis in v-Ki-ras-transformed NIH3T3 fibroblasts. The Ca2+ oscillations were inhibited by the addition of a specific antagonist for subtype 2 of BK receptors (B2 receptor), not the antagonist for B1 receptor. Decrease of the extracellular Ca2+ concentration suppressed the [Ca2+]i oscillations and application of thapsigargin dissipated the [Ca2+]i oscillations. These findings suggest that the continuous activation of B2 receptor leading to the fluctuations of both Ca2+ influx which refills the internal Ca2+ stores, and Ca2+ mobilization from the internal stores, is essential to the occurrence of the [Ca2+]i oscillations in these cells.
采用单细胞钙分析技术,在v-Ki-ras转化的NIH3T3成纤维细胞中研究了缓激肽(BK)诱导的细胞内钙振荡的调节。BK受体2型(B2受体)的特异性拮抗剂可抑制钙振荡,而B1受体拮抗剂则无此作用。细胞外钙浓度降低会抑制细胞内钙浓度([Ca2+]i)振荡,应用毒胡萝卜素可消除[Ca2+]i振荡。这些发现表明,B2受体的持续激活导致补充细胞内钙储存的钙内流和细胞内钙库释放钙的波动,这对于这些细胞中[Ca2+]i振荡的发生至关重要。