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缓激肽对培养的肾上皮(MDCK)细胞胞质Ca2+浓度的诱发调节作用。

Bradykinin-evoked modulation of cytosolic Ca2+ concentrations in cultured renal epithelial (MDCK) cells.

作者信息

Pidikiti N, Gamero D, Gamero J, Hassid A

出版信息

Biochem Biophys Res Commun. 1985 Jul 31;130(2):807-13. doi: 10.1016/0006-291x(85)90488-7.

Abstract

We have investigated the effect of bradykinin on cytosolic Ca2+ concentrations of renal MDCK cells cultured as monolayers. Bradykinin rapidly (within 5 to 20 s) increased cytosolic Ca2+ concentrations, measured by using the fluorescent indicator quin-2, from the basal value of 103 nM to a maximal value of 578 nM at about 10(-8) M bradykinin. The increase of Ca2+ was transient, returning to baseline within 1.5 to 2 min. The transient response appeared to be due to cell desensitization rather than peptide degradation. Previously desensitized cells could be resensitized after a 10 min incubation in the absence of bradykinin. The removal of extracellular Ca2+ or the addition of verapamil did not have a major effect on the maximal bradykinin-evoked changes of Ca2+, suggesting that Ca2+ released from intracellular stores plays a pivotal role in this process. Bradykinin-evoked Ca2+ metabolism may play an important role as modulator of the cellular functions of MDCK cells.

摘要

我们研究了缓激肽对单层培养的肾MDCK细胞胞质Ca2+浓度的影响。使用荧光指示剂喹啉-2测量,缓激肽能迅速(5至20秒内)将胞质Ca2+浓度从103 nM的基础值提高到约10(-8) M缓激肽时的最大值578 nM。Ca2+的增加是短暂的,在1.5至2分钟内恢复到基线。这种短暂反应似乎是由于细胞脱敏而非肽降解所致。先前脱敏的细胞在无缓激肽的情况下孵育10分钟后可重新致敏。去除细胞外Ca2+或添加维拉帕米对缓激肽引起Ca2+的最大变化没有重大影响,表明从细胞内储存释放的Ca2+在此过程中起关键作用。缓激肽诱发的Ca2+代谢可能作为MDCK细胞细胞功能的调节剂发挥重要作用。

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