Shima S, Itirai M, Asakura M
Naunyn Schmiedebergs Arch Pharmacol. 1980 May;312(1):19-22. doi: 10.1007/BF00502568.
Tolerance to catecholamines in the beta-adrenergic and dopaminergic receptor-adenylate cyclase system from the rat prostatic membrane has been studied. Preincubation of the tissue with isoproterenol produced not only a decrease in beta-adrenergic receptors and its sensitive adenylate cyclase activity, but also a reduction in dopaminergic response. Similarly, exposure to dopamine resulted in a decline both of isoproterenol- and dopamine-stimulated adenylate cyclase activity. A beta adrenergic antagonist, propranolol, exclusively blocked desensitization in the beta-adrenergic and dopaminergic adenylate cyclase system caused by isoproterenol, while dopamine-induced refractoriness was prevented by a dopaminergic antagonist, haloperidol. These results suggest that desensitization of the beta-adrenergic and dopaminergic adenylate cyclase system begins on receptor-occupation by its specific agonist.
对大鼠前列腺膜β-肾上腺素能和多巴胺能受体-腺苷酸环化酶系统中儿茶酚胺耐受性的研究。用异丙肾上腺素对组织进行预孵育,不仅会使β-肾上腺素能受体及其敏感的腺苷酸环化酶活性降低,还会使多巴胺能反应减弱。同样,暴露于多巴胺会导致异丙肾上腺素和多巴胺刺激的腺苷酸环化酶活性均下降。β-肾上腺素能拮抗剂普萘洛尔专门阻断了异丙肾上腺素引起的β-肾上腺素能和多巴胺能腺苷酸环化酶系统的脱敏作用,而多巴胺诱导的不应性则被多巴胺能拮抗剂氟哌啶醇所阻止。这些结果表明,β-肾上腺素能和多巴胺能腺苷酸环化酶系统的脱敏作用始于其特异性激动剂占据受体。