Tanaka T, Tani S
Faculty of Pharmaceutical Sciences, Josai University, Saitama, Japan.
Biol Pharm Bull. 1994 Mar;17(3):415-8. doi: 10.1248/bpb.17.415.
We examined the inhibitory effect of somatostatin on pepsinogen secretion using isolated rat gastric chief cells. Secretin and forskolin significantly increased not only pepsinogen secretion from chief cells but also cellular cAMP accumulation in a dose-dependent fashion. Somatostatin significantly inhibited secretin- and forskolin-induced pepsinogen secretion and secretin-induced cellular cAMP accumulation. However, forskolin-induced cellular cAMP accumulation was not inhibited by somatostatin. The inhibitory effect of somatostatin on secretin-induced pepsinogen secretion was abolished by pretreatment with pertussis toxin, but inhibition of forskolin-, carbachol- and cholecystokinin octapeptide-induced pepsinogen secretion was not. These results suggest that somatostatin inhibits pepsinogen secretion in two ways, one is closely related to the pertussis toxin-sensitive G-protein and the other is not determined.
我们使用分离的大鼠胃主细胞研究了生长抑素对胃蛋白酶原分泌的抑制作用。促胰液素和福斯高林不仅以剂量依赖的方式显著增加了主细胞的胃蛋白酶原分泌,还增加了细胞内cAMP的积累。生长抑素显著抑制促胰液素和福斯高林诱导的胃蛋白酶原分泌以及促胰液素诱导的细胞内cAMP积累。然而,生长抑素并未抑制福斯高林诱导的细胞内cAMP积累。生长抑素对促胰液素诱导的胃蛋白酶原分泌的抑制作用可被百日咳毒素预处理消除,但对福斯高林、卡巴胆碱和八肽胆囊收缩素诱导的胃蛋白酶原分泌的抑制作用则未被消除。这些结果表明,生长抑素以两种方式抑制胃蛋白酶原分泌,一种与百日咳毒素敏感的G蛋白密切相关,另一种尚不确定。