Chevillard C, Mathieu M N
Eur J Pharmacol. 1979 Jul 1;56(4):371-8. doi: 10.1016/0014-2999(79)90268-1.
Alterations of hypotensive responses to dopamine by antagonists were characterized in alpha-blocked, anaesthetized rats. Responses were not affected by d-propranolol (0.1 mg/kg) whereas d,1-propranolol (0.1 mg/kg) or haloperidol (1.0 mg/kg) attenuated them; higher doses of inhibitors (1.0 mg/kg; 5.0 mg/kg, respectively) failed to produce a higher inhibition, but combinations of low doses abolished the depressor responses. In adrenalectomized rats, hypotensive responses decreased; haloperidol always attenuated the responses while d,1-propranolol became ineffective. Dopamine produced an enhancement of plasma adrenaline and noradrenaline levels, which was decreased by d,1-propranolol and increased by haloperidol. The data suggest that in rats the depressor component of dopamine is due to activation of both dopaminergic and beta-adrenoceptors. The beta component appears to be due to the release of adrenaline. The results also support the concept of the existence in sympathetic nerve endings and adrenal glands of stimulatory beta-adrenergic and inhibitory dopaminergic prejunctional receptors.
在α受体阻断、麻醉的大鼠中研究了拮抗剂对多巴胺降压反应的影响。反应不受d-普萘洛尔（0.1mg/kg）影响，而d,1-普萘洛尔（0.1mg/kg）或氟哌啶醇（1.0mg/kg）可减弱反应；更高剂量的抑制剂（分别为1.0mg/kg；5.0mg/kg）未能产生更高的抑制作用，但低剂量组合可消除降压反应。在肾上腺切除的大鼠中，降压反应降低；氟哌啶醇始终减弱反应，而d,1-普萘洛尔则无效。多巴胺可使血浆肾上腺素和去甲肾上腺素水平升高，d,1-普萘洛尔可使其降低，氟哌啶醇可使其升高。数据表明，在大鼠中，多巴胺的降压成分是由于多巴胺能和β-肾上腺素能受体的激活。β成分似乎是由于肾上腺素的释放。结果还支持在交感神经末梢和肾上腺中存在刺激性β-肾上腺素能和抑制性多巴胺能突触前受体的概念。
