Gaginella T S, Phillips S F, Dozois R R, Go V L
Gastroenterology. 1978 Jan;74(1):11-5.
The mechanism by which intestinal secretagogues evoke fluid secretion in the small bowel and colon has been suggested to involve mucosal adenylate cyclase. Adenylate cyclase activity was assayed by conversion of [32P]ATP to [32P]cyclic AMP in a system of pure epithelial cells isolated from the small intestine of the hamster by vibration in buffer. Several gastrointestinal hormones were tested for their capacity to stimulate adenylate cyclase; vasoactive intestinal peptide and impure cholecystokinin-pancreozymin (but not the 99% pure preparation or pure cholecystokinin octapeptide) were potent stimuli, but pentagastrin, glucagon, secretin, and gastric inhibitory peptide were impotent. Two prostaglandins, PGE1 and PGE2, were potent stimuli of adenylate cyclase. Two other compounds that provoke intestinal secretion of fluid, deoxycholic acid and ricinoleic acid (castor oil), were ineffective stimuli of adenylate cyclase. These experiments do not support a clear-cut relationship between a compound's ability to stimulate adenylate cylase and its activity as an intestinal secretagogue.
肠促分泌素引起小肠和结肠液体分泌的机制已被认为与粘膜腺苷酸环化酶有关。通过在缓冲液中振动从仓鼠小肠分离的纯上皮细胞系统中，将[32P]ATP转化为[32P]环磷酸腺苷来测定腺苷酸环化酶活性。测试了几种胃肠激素刺激腺苷酸环化酶的能力；血管活性肠肽和不纯的胆囊收缩素-促胰酶素（但不是99%纯制剂或纯胆囊收缩素八肽）是有效的刺激物，但五肽胃泌素、胰高血糖素、促胰液素和胃抑制肽无效。两种前列腺素PGE1和PGE2是腺苷酸环化酶的有效刺激物。另外两种引起肠液分泌的化合物脱氧胆酸和蓖麻油酸（蓖麻油），是腺苷酸环化酶的无效刺激物。这些实验不支持化合物刺激腺苷酸环化酶的能力与其作为肠促分泌素的活性之间存在明确关系。
