Constantine J W, Gunnell D, Weeks R A
Eur J Pharmacol. 1980 Sep 5;66(4):281-6. doi: 10.1016/0014-2999(80)90460-4.
Prazosin inhibited contractions of isolated electrically stimulated dog pulmonary artery preincubated with (-)-7-3H-norepinephrine, but had no effect on 3H-overflow, whereas yohimbine enhanced both responses. In pithed dogs the cumulative doses of yohimbine required for 50% inhibition of the pressor effects of clonidine, phenylephrine and norepinephrine were 23, 188 and 35 micrograms/kg i.v., and those for prazosin were 9, 1.5 and 5 micrograms/kg i.v., respectively. The agonists could be ranked in pairs depending on the extent to which the antagonists discriminated members of the pair: clonidine-phenylephrine > phenylephrine-norepinephrine > clonidine-norepinephrine. The results suggest that pressor effects in dogs are mediated by both alpha 1- and alpha 2-vascular (i.e. postsynaptic) adrenoceptors.
哌唑嗪抑制预先用(-)-7-3H-去甲肾上腺素孵育的离体电刺激犬肺动脉的收缩,但对3H-溢出无影响,而育亨宾增强了这两种反应。在脊髓麻醉犬中,50%抑制可乐定、去氧肾上腺素和去甲肾上腺素升压作用所需的育亨宾累积剂量分别为静脉注射23、188和35微克/千克,而哌唑嗪的累积剂量分别为静脉注射9、1.5和5微克/千克。根据拮抗剂区分配对成员的程度,激动剂可以成对排序:可乐定-去氧肾上腺素>去氧肾上腺素-去甲肾上腺素>可乐定-去甲肾上腺素。结果表明,犬的升压作用由α1和α2血管(即突触后)肾上腺素能受体介导。