Modulation of bradykinin-induced intracellular Ca2+ oscillations in v-Ki-ras-transformed fibroblasts.
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.
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Laboratory of Cellular and Molecular Oncology, Shanghai Institute of Cell Biology, Chinese Academy of Sciences.
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Xu
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D016475:3T3 Cells / Q000378:metabolism*; D000818:Animals; D001920:Bradykinin / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D065168:Bradykinin Receptor Antagonists; D015220:Calcium Channels / Q000187:drug effects*; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D011905:Genes, ras; D051379:Mice; D013729:Terpenes / Q000494:pharmacology; D019284:Thapsigargin
D065168:Bradykinin Receptor Antagonists; D015220:Calcium Channels; D013729:Terpenes; C053748:B 4162; C051090:bradykinin, Leu(8)-des-Arg(9)-; D019284:Thapsigargin; D000252:Calcium-Transporting ATPases; D001920:Bradykinin