Mössner J, Fischbach W
Klin Wochenschr. 1986 Jun 2;64(11):489-98. doi: 10.1007/BF01713055.
Peptides may act on the same receptor they regulate or on another receptor by causing regulations via receptor interactions. These receptor regulations include changes of receptor affinity and capacity. Receptor capacity is regulated by internalization, recycling, degradation, synthesis, and modification of bioavailability without migration of the receptor. Examples for those regulations, mostly based on experiments with isolated pancreatic acini from the rat, mouse, or guinea pig, are given. For the CCK receptor these examples include complex regulations of this receptor by CCK itself, bringing into discussion the hypothesis of negative cooperativity and the two-site receptor model, desensitization of the receptor by CCK, in vivo CCK influences on its receptor, and insulin receptor/CCK receptor interactions. For the insulin receptor the physiological significance of "up and down regulation" of this receptor by insulin itself is discussed. For the IGF receptors and the EGF receptor CCK-induced, Ca2+-mediated regulation of receptor internalization are another type of regulation with unknown physiological and pathophysiological significance. Finally CCK-induced, Ca2+-mediated regulation of somatostatin receptor capacity and affinity are mentioned. It is postulated that those regulations play an important role in influencing the biological effect of hormones and that knowledge about them may improve our understanding of pathophysiology.
肽可通过受体相互作用引起调节,作用于它们所调节的同一受体或另一受体。这些受体调节包括受体亲和力和容量的变化。受体容量通过内化、再循环、降解、合成以及生物利用度的修饰来调节,而受体并不迁移。给出了这些调节的实例,大多基于对大鼠、小鼠或豚鼠分离胰腺腺泡的实验。对于CCK受体,这些实例包括CCK自身对该受体的复杂调节,引发了负协同性假说和双位点受体模型的讨论,CCK使受体脱敏,体内CCK对其受体的影响,以及胰岛素受体/CCK受体相互作用。对于胰岛素受体,讨论了胰岛素自身对该受体“上调和下调”的生理意义。对于IGF受体和EGF受体,CCK诱导的、Ca2+介导的受体内化调节是另一种具有未知生理和病理生理意义的调节类型。最后提到了CCK诱导的、Ca2+介导的生长抑素受体容量和亲和力的调节。据推测,这些调节在影响激素的生物学效应中起重要作用,并且有关它们的知识可能会增进我们对病理生理学的理解。