Shima S, Komoriyama K, Hirai M, Kouyama H
J Biol Chem. 1983 Feb 25;258(4):2083-6.
Exposure of rat prostatic tissues to isoproterenol resulted in rapid desensitization of their catecholamine-sensitive adenylate cyclase which was associated with reduction of available beta-adrenoceptors and a loss of guanine nucleotide-mediated regulation of agonist binding to these receptors. The effect of isoproterenol treatment on responsiveness of the adenylate cyclase was prevented by acetylcholine, high potassium ion, or the calcium ionophore A23187. Preservation of responsiveness was not accompanied by maintenance of available beta-adrenoceptors or maintenance of guanine nucleotide regulation of agonist bindings. These results suggest that the lesion of the guanine nucleotide regulating components coupled to the catalytic moiety of the enzyme complex is a crucial factor in the desensitization of catecholamine-sensitive adenylate cyclase and the preservation of enzyme reaction could be accomplished by agents increasing intracellular calcium, which in turn, maintain the nucleotide regulatory components coupling to the cyclase in a protective environment from desensitization.
将大鼠前列腺组织暴露于异丙肾上腺素会导致其儿茶酚胺敏感性腺苷酸环化酶迅速脱敏，这与可用β-肾上腺素能受体的减少以及鸟嘌呤核苷酸介导的激动剂与这些受体结合调节的丧失有关。乙酰胆碱、高钾离子或钙离子载体A23187可阻止异丙肾上腺素处理对腺苷酸环化酶反应性的影响。反应性的保留并不伴随着可用β-肾上腺素能受体的维持或激动剂结合的鸟嘌呤核苷酸调节的维持。这些结果表明，与酶复合物催化部分偶联的鸟嘌呤核苷酸调节成分的损伤是儿茶酚胺敏感性腺苷酸环化酶脱敏的关键因素，而增加细胞内钙的试剂可实现酶反应的保留，进而使与环化酶偶联的核苷酸调节成分在免受脱敏的保护环境中得以维持。
