Nakano O, Sakamoto C, Nishisaki H, Konda Y, Matsuda K, Wada K, Nagao M, Matozaki T
Second Department of Internal Medicine, Kobe University School of Medicine, Japan.
Life Sci. 1990;47(7):647-54. doi: 10.1016/0024-3205(90)90577-e.
In isolated guinea pig gastric chief cells, sodium fluoride (NaF) stimulated a monophasic increase in diacylglycerol accumulation, while cholecystokinin (CCK) strongly stimulated its biphasic accumulation. NaF evoked an increase in initial Ca2+ influx rate with a slow increase in intracellular free Ca2+ concentration [( Ca2+]i), while CCK stimulated a rapid increase in [Ca2+]i followed by a late sustained phase of the [Ca2+]i increase. Lanthanum chloride (La3+) effectively blocked NaF-stimulated increase in [Ca2+]i, but it blocked only CCK-stimulated late sustained phase of [Ca2+]i increase. The effect of NaF on pepsinogen secretion was enhanced in the presence of 100 microM AlCl3. Furthermore, pertussis toxin did not affect NaF-evoked diacylglycerol accumulation at all. These results suggest that NaF may activate a pertussis-toxin insensitive guanine nucleotide regulatory protein (G protein) coupled to a signal transducing mechanism which seems to be distinct from that activated by CCK, thereby inducing increases in diacylglycerol accumulation, Ca2+ influx and pepsinogen secretion in guinea pig gastric chief cells.
在分离的豚鼠胃主细胞中,氟化钠(NaF)刺激二酰基甘油积累呈单相增加,而胆囊收缩素(CCK)强烈刺激其二相积累。NaF引起初始Ca2+内流速率增加,细胞内游离Ca2+浓度[Ca2+]i缓慢升高,而CCK刺激[Ca2+]i迅速升高,随后是[Ca2+]i升高的晚期持续阶段。氯化镧(La3+)有效阻断了NaF刺激的[Ca2+]i升高,但仅阻断了CCK刺激的[Ca2+]i升高的晚期持续阶段。在100 microM AlCl3存在下,NaF对胃蛋白酶原分泌的作用增强。此外,百日咳毒素对NaF引起的二酰基甘油积累完全没有影响。这些结果表明,NaF可能激活一种对百日咳毒素不敏感的鸟嘌呤核苷酸调节蛋白(G蛋白),该蛋白与一种信号转导机制偶联,这种信号转导机制似乎与CCK激活的机制不同,从而导致豚鼠胃主细胞中二酰基甘油积累、Ca2+内流和胃蛋白酶原分泌增加。