CA2+-DEPENDENT K+ CHANNEL ACTIVITY IN RAT GLIOMA-CELLS INDUCED BY BRADYKININ STIMULATION AND BY INOSITOL 1,4,5-TRISPHOSPHATE INJECTION

被引:3
|
作者
BINMOLLER, FJ
REISER, G
机构
[1] Physiologisch-chemisches Institut, Universität Tübingen, Tübingen, 72076
关键词
BRADYKININ; GLIOMA; NEUROPEPTIDE; INOSITOLPHOSPHATE; K+ CHANNEL;
D O I
10.1007/BF00711561
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
1. A glial cell line derived from C6 rat glioma eels has been shown previously to respond to extracellular pulses of bradykinin or intracellular injection of inositol 1,4,5-trisphosphate (Ins-P-3) with a slow hyperpolarizing response due to activation of a K+ current (G. Reiser ef al., Brain Res. 506, 205-214; 1990). 2. We determined the ensuing single-channel activity, which is most likely caused by Ca2+ released from internal stores after bradykinin stimulation. Bradykinin-activated channels were selectively permeable to K+, but not to Na+ or to Cl-, and exhibited conductances of mainly 40 and 50 pS. In glioma cells the same type of channel was activated by intracellular injection of Ins-P-3 and by extracellular bradykinin pulses.
引用
收藏
页码:615 / 624
页数:10
相关论文
共 50 条
  • [21] Feedback regulation of the inositol 1,4,5-trisphosphate receptor/Ca2+ release channel by Ca2+
    Michikawa, T
    Mikoshiba, K
    CONTROL AND DISEASES OF SODIUM DEPENDENT TRANSPORT PROTEINS AND ION CHANNELS, 2000, 1208 : 217 - 220
  • [22] Inositol 1,4,5-trisphosphate receptor/Ca2+ channel modulatory role of chromogranins A and B
    Yoo, SH
    So, SH
    Huh, YH
    Park, HY
    CHROMAFFIN CELL: TRNSMITTER BIOSYNTHESIS, STORAGE, RELEASE, ACTIONS, AND INFORMATICS, 2002, 971 : 300 - 310
  • [23] BRADYKININ OR INOSITOL 1,4,5-TRISPHOSPHATE INCREASE CA-2+ DEPENDENT ACETYLCHOLINE SECRETION FROM NG108-15 NEUROBLASTOMA-GLIOMA HYBRID-CELLS
    HIGASHIDA, H
    FEDERATION PROCEEDINGS, 1986, 45 (06) : 1690 - 1690
  • [24] Thromboxane A(2) mediates bradykinin stimulation of inositol 1,4,5-trisphosphate production and intracellular calcium mobilization in neonatal rat cardiomyocytes.
    Rabito, SF
    Nakamura, F
    Minshall, RD
    LeBreton, GC
    HYPERTENSION, 1996, 28 (03) : P163 - P163
  • [25] INJECTED INOSITOL 1,4,5-TRISPHOSPHATE ACTIVATES CA-2+-SENSITIVE K+ CHANNELS IN THE PLASMALEMMA OF EREMOSPHAERA-VIRIDIS
    FORSTER, B
    FEBS LETTERS, 1990, 269 (01) : 197 - 201
  • [26] INOSITOL 1,4,5-TRISPHOSPHATE AND INOSITOL 1,3,4-TRISPHOSPHATE FORMATION IN CA-2+-MOBILIZING-HORMONE-ACTIVATED CELLS
    BURGESS, GM
    MCKINNEY, JS
    IRVINE, RF
    PUTNEY, JW
    BIOCHEMICAL JOURNAL, 1985, 232 (01) : 237 - 243
  • [27] Synergistic actions of diacylglycerol and inositol 1,4,5 trisphosphate for Ca2+-dependent inactivation of TRPC7 channel
    Zhang, Hua
    Inoue, Ryuji
    Shi, Juan
    Jin, Xiao-hang
    Li, Yun-qing
    ACTA PHARMACOLOGICA SINICA, 2008, 29 (01) : 90 - 97
  • [28] Synergistic actions of diacylglycerol and inositol 1,4,5 trisphosphate for Ca2+-dependent inactivation of TRPC7 channel
    Hua Zhang
    Ryuji Inoue
    Juan Shi
    Xiao-hang Jin
    Yun-qing Li
    Acta Pharmacologica Sinica, 2008, 29 : 90 - 97
  • [29] Ca2+-induced Ca2+ release by activation of inositol 1,4,5-trisphosphate receptors in primary pancreatic β-cells
    Dyachok, O
    Tufveson, G
    Gylfe, E
    CELL CALCIUM, 2004, 36 (01) : 1 - 9
  • [30] BRADYKININ-INDUCED CA2+-INFLUX INTO CULTURED AORTIC ENDOTHELIAL-CELLS IS NOT REGULATED BY INOSITOL 1,4,5-TRISPHOSPHATE OR INOSITOL 1,3,4,5-TETRAKISPHOSPHATE
    GRAIER, WF
    SCHMIDT, K
    KUKOVETZ, WR
    SECOND MESSENGERS AND PHOSPHOPROTEINS, 1991, 13 (04): : 187 - 197