Kubo T, Misu Y
Can J Physiol Pharmacol. 1981 Jun;59(6):615-7. doi: 10.1139/y81-094.
The administration of nicotine into the cisterna magna evoked a delayed depressor effect with an initial pressor effect in anaesthetized rats. The depressor response was accompanied by a bradycardia. The cardiovascular effects of nicotine were abolished after intracisternal administration of hexamethonium but not after atropine given via the same route. Intravenous administration of methylatropine abolished the bradycardic response to nicotine but did not affect the blood pressure responses. The pressor effect of nicotine was abolished by intravenous administration of phenoxybenzamine. The cardiovascular effects of nicotine injected intracisternally were abolished when the diffusion of nicotine onto an area around the area postrema was interrupted using a polyethylene tube. In contrast, nicotine applied to the area produced a marked pressor--depressor response. It is concluded that the cardiovascular responses to intracisternal administration of nicotine result from the activation of central nicotinic receptor sites that may be present around the area postrema.
向麻醉大鼠的脑大池注射尼古丁会引发一种延迟性降压效应，并伴有初始升压效应。降压反应伴有心动过缓。脑池内注射六甲铵后，尼古丁的心血管效应消失，但通过相同途径注射阿托品后，该效应并未消失。静脉注射甲基阿托品可消除对尼古丁的心动过缓反应，但不影响血压反应。静脉注射酚苄明可消除尼古丁的升压效应。当使用聚乙烯管中断尼古丁向最后区周围区域的扩散时，脑池内注射尼古丁的心血管效应消失。相反，将尼古丁应用于该区域会产生明显的升压 - 降压反应。结论是，脑池内注射尼古丁引起的心血管反应是由最后区周围可能存在的中枢烟碱受体部位的激活所致。
