Marcou M, Munday K A, Horn N, Woodruff G N
Arch Int Pharmacodyn Ther. 1982 Sep;259(1):59-71.
Dopamine and isoprenaline have been examined for their effects on guinea-pig renal blood flow in vivo and on cAMP production in a mainly isolated glomeruli/blood vessel preparation in vitro. The renal vasodilatation caused by both of these drugs can be differentiated by the use of specific antagonists, sulpiride blocking the effects of dopamine, and propranolol the vasodilatation produced by isoprenaline. Similarly, both drugs stimulated cAMP production, isoprenaline being much more active than dopamine (1000X) in this respect. Again, the dopamine antagonist fluphenazine specifically inhibited the dopamine-induced cAMP increases whilst the beta blocker atenolol blocked the rise in cAMP due to isoprenaline but not that due to dopamine. Sulpiride although potently inhibiting dopamine-induced renal vasodilatation was without effect on dopamine-stimulated cAMP levels. This result is similar to that reported in the CNS where sulpiride blocks dopamine activity in a variety of tests but is without effect on the dopamine-stimulated adenylate cyclase. Two dopamine agonists, ADTN and SKF 38393 were tested, and in both preparations had potent dopaminergic activity although SKF 38393 exhibited characteristics of a partial agonist on the adenylate cyclase model.
已对多巴胺和异丙肾上腺素在体内对豚鼠肾血流量的影响以及在体外主要分离的肾小球/血管制剂中对环磷酸腺苷（cAMP）产生的影响进行了研究。这两种药物引起的肾血管舒张作用可通过使用特异性拮抗剂来区分，舒必利可阻断多巴胺的作用，普萘洛尔可阻断异丙肾上腺素产生的血管舒张作用。同样，两种药物均刺激了cAMP的产生，在这方面异丙肾上腺素比多巴胺活跃得多（1000倍）。同样，多巴胺拮抗剂氟奋乃静特异性抑制多巴胺诱导的cAMP增加，而β受体阻滞剂阿替洛尔阻断因异丙肾上腺素引起的cAMP升高，但不阻断因多巴胺引起的cAMP升高。舒必利虽然能有效抑制多巴胺诱导的肾血管舒张，但对多巴胺刺激的cAMP水平没有影响。这一结果与中枢神经系统中报道的结果相似，在中枢神经系统中，舒必利在各种试验中均阻断多巴胺活性，但对多巴胺刺激的腺苷酸环化酶没有影响。测试了两种多巴胺激动剂，ADTN和SKF 38393，在两种制剂中它们均具有强大的多巴胺能活性，尽管SKF 38393在腺苷酸环化酶模型上表现出部分激动剂的特征。
