Menozzi D, Stark H A, Martinez J, Jensen R T, Gardner J D
Digestive Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD 20892.
Peptides. 1989 Mar-Apr;10(2):337-41. doi: 10.1016/0196-9781(89)90040-5.
CCK-8-induced desensitization of carbachol-stimulated amylase secretion occurred over a range of concentrations of CCK-8 that occupy low affinity CCK receptors. CCK-JMV-180 [BOC-Tyr(SO3)-Nle-Gly-Trp-Nle-Asp-2-phenylethylester] at concentrations up to 1 microM did not cause desensitization of enzyme secretion; however, the peptide was able to inhibit CCK-8-induced desensitization. Analysis of the relationship between receptor occupation and CCK-8-induced desensitization caused by CCK-8 and CCK-JMV-180 in combination also indicated that CCK-8-induced desensitization of carbachol-stimulated amylase secretion is caused by occupation of low affinity CCK receptors.
胆囊收缩素-8（CCK-8）诱导的对卡巴胆碱刺激的淀粉酶分泌的脱敏作用，在占据低亲和力CCK受体的一系列CCK-8浓度范围内发生。浓度高达1微摩尔的CCK-JMV-180 [叔丁氧羰基-酪氨酸（磺酸）-亮氨酸-甘氨酸-色氨酸-亮氨酸-天冬氨酸-2-苯乙酯] 不会引起酶分泌的脱敏；然而，该肽能够抑制CCK-8诱导的脱敏。对CCK-8和CCK-JMV-180联合作用下受体占据与CCK-8诱导的脱敏之间关系的分析也表明，CCK-8诱导的对卡巴胆碱刺激的淀粉酶分泌的脱敏是由低亲和力CCK受体的占据引起的。
