Tanaka T, Miyadera K, Tani S
Faculty of Pharmaceutical Sciences, Josai University, Saitama, Japan.
Biol Pharm Bull. 1993 Aug;16(8):767-70. doi: 10.1248/bpb.16.767.
Gastric chief cells were isolated from the rat stomach in an attempt to identify those involved in the mechanism of action of somatostatin on pepsinogen secretion. The effects of several kinds of secretagogues on cytosolic free Ca2+ concentration ([Ca2+]i) were examined in the rat chief cells. Carbachol and cholecystokinin octapeptide (CCK-8) markedly induced [Ca2+]i increase, while histamine, gastrin I and secretin did not. Carbachol and CCK-8 also stimulated pepsinogen secretion. A similar dose-response relationship was seen in carbachol- and CCK-8-induced [Ca2+]i increase and pepsinogen secretion. Somatostatin did not inhibit carbachol- or CCK-8-induced [Ca2+]i increase, but did inhibit carbachol- and CCK-8-induced pepsinogen secretion by 30 and 50%, respectively.
为了确定参与生长抑素对胃蛋白酶原分泌作用机制的细胞,从大鼠胃中分离出胃主细胞。研究了几种促分泌素对大鼠主细胞胞质游离钙离子浓度([Ca2+]i)的影响。卡巴胆碱和八肽胆囊收缩素(CCK-8)显著诱导[Ca2+]i升高,而组胺、胃泌素I和促胰液素则无此作用。卡巴胆碱和CCK-8也刺激胃蛋白酶原分泌。在卡巴胆碱和CCK-8诱导的[Ca2+]i升高与胃蛋白酶原分泌中观察到类似的剂量反应关系。生长抑素不抑制卡巴胆碱或CCK-8诱导的[Ca2+]i升高,但分别抑制卡巴胆碱和CCK-8诱导的胃蛋白酶原分泌30%和50%。