Mouillé P, Huchet A M, Chelly J, Schmitt H
C R Seances Acad Sci D. 1979 Feb 5;288(5):551-4.
In Dogs anaesthetized with pentobarbital (30 mg . kg-1), N-butylnorsympathone (20 mg . kg-1 i.v.) reduced the bradycardia induced by stimulating the cardiac nerve (1, 2, 5, 10 Hz). Phentolamine (1 mg . kg-1 i.v.) or yohimbine (0.3 mg . kg-1 i.v.), two potent alpha-adrenoceptor blocking agents known to block presynaptic alpha-adrenoceptor induced a recovery of the effect of cardiac nerve stimulation. Prazosine (0.050 mg . kg-1 i.v.) an alpha-adrenoceptor blocking agent known to be ineffective on presynaptic alpha-adrenoceptors did not induce a recovery. However neither phentolamine or yohimbine were able to prevent the effects of N-butylnorsympathone. Neither haloperidol (0.050 to 2 mg . kg-1 i.v.) or pimozide (0.20 to 1 mg . kg-1 i.v.) induced a recovery or prevented the effects of N-butylnorsympathone. These results suggest that N-butylnorsympathone may stimulate presynaptic receptors which do not resemble classical presynaptic alpha-adrenoceptors or dopamine receptors.
在用戊巴比妥(30毫克·千克-1)麻醉的犬中,N-丁基去甲交感酮(20毫克·千克-1静脉注射)可减轻刺激心脏神经(1、2、5、10赫兹)所诱发的心动过缓。酚妥拉明(1毫克·千克-1静脉注射)或育亨宾(0.3毫克·千克-1静脉注射),这两种已知可阻断突触前α-肾上腺素能受体的强效α-肾上腺素能受体阻断剂,可使心脏神经刺激的效应恢复。哌唑嗪(0.050毫克·千克-1静脉注射),一种已知对突触前α-肾上腺素能受体无效的α-肾上腺素能受体阻断剂,并未引起效应恢复。然而,酚妥拉明或育亨宾均无法预防N-丁基去甲交感酮的作用。氟哌啶醇(0.050至2毫克·千克-1静脉注射)或匹莫齐特(0.20至1毫克·千克-1静脉注射)均未引起效应恢复或预防N-丁基去甲交感酮的作用。这些结果表明,N-丁基去甲交感酮可能刺激的突触前受体与经典的突触前α-肾上腺素能受体或多巴胺受体不同。