Kobinger W, Pichler L
Eur J Pharmacol. 1975 Jan;30(1):56-62. doi: 10.1016/0014-2999(75)90202-2.
Rats were decerebrated and treated with a beta-adrenoceptor blocker (toliprolol, Kö 592, 5 mg/kg). Increases of blood pressure were repeatedly elicited by i.v. injection of angiotensin (0.03-0. 125 mug/kg) ant eh accompanying reflex bradycardia was measured. The vagally mediated reflex bradycardia was significantly increased by clonidine, 3o mug/kg i.v., in non-pretreated animals as well as after pretreatment with reserpine (7.5 mg/kg s.c., 20 hr) and alpha-methyl-p-tyrosine-methylester (250 mg/kg i.p., 5 hr), separately or in combination. The facilitatory effect of clonidine was antagonized in all groups by i.v. injection of the alpha-adrenoceptor blocking drugs, phentolamine (5 mg/kg) and piperoxan (1 mg/kg). In the control periods before clonidine, reflex bradycardia was similar in pretreated animals to that in animals without pretreatment. It was concluded therefore that catecholamines have no essential transmitter functions in the cardiodepressor reflex loop. Therefore, the action of clonidine on cardiovascular centers in the medulla is independent of endogenous noradrenaline storage and synthesis. A direct effect is assumed on central alpha-adrenoceptors, which have a modulatory 'effector' function on the cardiodepressor reflex.
将大鼠大脑切除并给予β-肾上腺素能受体阻滞剂（托利洛尔，Kö 592，5毫克/千克）。通过静脉注射血管紧张素（0.03 - 0.125微克/千克）反复引发血压升高，并测量伴随的反射性心动过缓。在未预处理的动物以及分别或联合用利血平（7.5毫克/千克，皮下注射，20小时）和α-甲基对酪氨酸甲酯（250毫克/千克，腹腔注射，5小时）预处理后，静脉注射30微克/千克可乐定可使迷走神经介导的反射性心动过缓显著增加。静脉注射α-肾上腺素能阻断药物酚妥拉明（5毫克/千克）和哌泊噻嗪（1毫克/千克）可拮抗可乐定在所有组中的促进作用。在给予可乐定之前的对照期，预处理动物的反射性心动过缓与未预处理动物相似。因此得出结论，儿茶酚胺在心脏抑制反射环中没有基本的递质功能。所以，可乐定对延髓心血管中枢的作用独立于内源性去甲肾上腺素的储存和合成。推测其对中枢α-肾上腺素能受体有直接作用，这些受体对心脏抑制反射具有调节“效应器”功能。
