Fong J C, Ho L T, Wang F F
Institute of Biochemistry, National Yang-Ming Medical College, Taipei, Taiwan, Republic of China.
Biochem Int. 1989 Dec;19(6):1165-72.
Forskolin was found to stimulate pepsinogen secretion from frog esophageal mucosa. The stimulation was dose-dependent and was accompanied with a great increase in tissue cAMP content. The response to forskolin mimicked the action of bethanechol and was not additive with bethanechol. The stimulatory effect of forskolin was inhibited by 50% in the presence of either atropine or tetrodotoxin. On the other hand, incubation in a calcium-free medium not only reduced the response to forskolin by 45% but also eliminated the influence of atropine and tetrodotoxin. These results indicate that forskolin may stimulate pepsinogen secretion from the frog esophageal mucosa via activating adenylate cyclase, and part of its effect may arise from eliciting acetylcholine release from the intrinsic neurons.
发现福斯高林可刺激青蛙食管黏膜分泌胃蛋白酶原。这种刺激呈剂量依赖性，并且伴随着组织中环磷酸腺苷（cAMP）含量的大幅增加。对福斯高林的反应模拟了氨甲酰甲胆碱的作用，且与氨甲酰甲胆碱的作用并非相加性。在存在阿托品或河豚毒素的情况下，福斯高林的刺激作用被抑制了50%。另一方面，在无钙培养基中孵育不仅使对福斯高林的反应降低了45%，还消除了阿托品和河豚毒素的影响。这些结果表明，福斯高林可能通过激活腺苷酸环化酶来刺激青蛙食管黏膜分泌胃蛋白酶原，其部分作用可能源于促使内在神经元释放乙酰胆碱。
