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百日咳毒素可抑制血管紧张素II和血清素诱导的大鼠主动脉培养平滑肌细胞中游离细胞质钙的升高。

Pertussis toxin inhibits the angiotensin II and serotonin-induced rise of free cytoplasmic calcium in cultured smooth muscle cells from rat aorta.

作者信息

Bruns C, Marmé D

出版信息

FEBS Lett. 1987 Feb 9;212(1):40-4. doi: 10.1016/0014-5793(87)81552-1.

Abstract

Angiotensin II, serotonin and K+-depolarization cause an increase in free cytoplasmic Ca2+ in cultured smooth muscle cells. The involvement of a guanine nucleotide-binding protein has been investigated by using pertussis toxin. When smooth muscle cells were pretreated with pertussis toxin angiotensin II and serotonin-induced rise of cytosolic Ca2+ was found to be significantly reduced whereas the Ca2+ influx mediated by K+-depolarization remained unchanged. These results suggest the participation of a guanine nucleotide-binding protein in the receptor-mediated rise of intracellular Ca2+.

摘要

血管紧张素II、血清素和钾离子去极化会导致培养的平滑肌细胞中游离细胞质钙离子增加。已通过使用百日咳毒素研究了鸟嘌呤核苷酸结合蛋白的参与情况。当平滑肌细胞用百日咳毒素预处理时,发现血管紧张素II和血清素诱导的细胞质钙离子升高显著降低,而由钾离子去极化介导的钙离子内流保持不变。这些结果表明鸟嘌呤核苷酸结合蛋白参与了受体介导的细胞内钙离子升高过程。

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