Gurtu S, Sharma D K, Sinha J N, Bhargava K P
Naunyn Schmiedebergs Arch Pharmacol. 1983 Jul;323(3):199-204. doi: 10.1007/BF00497663.
Microinjection of noradrenaline and clonidine into the nucleus ambiguus elicited dose-dependent bradycardia with insignificant alteration of blood pressure. Phenylephrine failed to elicit any cardiovascular effect. The bradycardic effects of noradrenaline and clonidine were antagonized by piperoxan but not by phenoxybenzamine. Adrenergic neurone blockade with local guanethidine pretreatment also abolished the response to clonidine. No significant cardiovascular effect of clonidine microinjection into the nucleus ambiguus was observed in bilaterally vagotomized animals. The baroreflex bradycardia induced by volume loading as abolished by yohimbine and piperoxan but not by phenoxybenzamine, microinjected bilaterally into the nucleus ambiguus. These results demonstrate the presence of cardioinhibitory, presynaptic alpha 2-adrenoceptors in the nucleus ambiguus and their involvement in baroreflex bradycardia.
向疑核微量注射去甲肾上腺素和可乐定可引起剂量依赖性心动过缓，血压无明显变化。去氧肾上腺素未能引起任何心血管效应。去甲肾上腺素和可乐定的心动过缓效应可被哌罗克生拮抗，但不能被酚苄明拮抗。局部胍乙啶预处理进行肾上腺素能神经元阻滞也可消除对可乐定的反应。在双侧迷走神经切断的动物中，未观察到向疑核微量注射可乐定有明显的心血管效应。双侧向疑核微量注射育亨宾和哌罗克生可消除容量负荷诱导的压力反射性心动过缓，但酚苄明无此作用。这些结果表明疑核中存在心脏抑制性突触前α2肾上腺素能受体，且它们参与压力反射性心动过缓。
