Initial bradykinin triggers calcium-induced calcium release in C6 glioma cells and its significance.
OBJECTIVE
To investigate the underlying mechanism for the selective modulation of the permeability of blood-tumor barrier (BTB) by small dose of bradykinin (BK).


METHODS
C6 glioma cells were treated with BK, and changes of intracellular nitric oxide (NO) and intracellular calcium level were measured with fluorescent spectrophotometer.


RESULTS
The initial application of BK easily triggered extracellular calcium influx, which resulted in intracellular calcium store release in C6 glioma cells. The above mechanism was also named ryanodine mediated calcium induced calcium release (CICR). We also detected a long-lasting intracellular NO elevation in C6 glioma cells upon BK treatment. Further study showed that ryanodine mediated CICR contributed greatly to the secondary NO elevation induced by BK treatment.


CONCLUSIONS
These results suggested that BK triggered CICR in C6 glioma cells and the associated NO generation might be the underlying mechanism for the selective modulation of BTB permeability by BK.
Wang
Yi-Bao
YB
Department of Neurosurgery, the First Affiliated Hospital of China Medical University, Shenyang 110001, China. cmuwyb@gmail.com
Liu
Yun-Hui
YH
D000818:Animals; D001920:Bradykinin / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D045744:Cell Line, Tumor; D005910:Glioma / Q000473:pathology; D007424:Intracellular Fluid / Q000187:drug effects*; D009569:Nitric Oxide / Q000378:metabolism; D051381:Rats; D012433:Ryanodine / Q000494:pharmacology; D013050:Spectrometry, Fluorescence / Q000379:methods; D013997:Time Factors
D012433:Ryanodine; D009569:Nitric Oxide; D001920:Bradykinin; D002118:Calcium