Connor H E, Drew G M, Finch L
J Pharm Pharmacol. 1982 Jan;34(1):22-6. doi: 10.1111/j.2042-7158.1982.tb04671.x.
The interactions between clonidine and the selective alpha 1- and alpha 2-adrenoceptor antagonists, prazosin and yohimbine, on the angiotensin-induced reflex vagal bradycardia have been investigated in propranolol-treated chloralose-anaesthetized cats. Clonidine (1-10 microgram intracisternally) had little effect on the pressor responses to angiotensin, only slightly increased the peak but markedly increased the duration of the reflex bradycardia. Neither prazosin nor yohimbine (200 microgram intracisternally of either antagonist) had any effect on the reflex bradycardia to angiotensin. Yohimbine greatly diminished the clonidine-induced potentiation of the response, but prazosin was without effect. Clonidine appears to potentiate the vagal reflex bradycardia by stimulating central alpha 2-adrenoceptors.
在普萘洛尔处理的、水合氯醛麻醉的猫身上,研究了可乐定与选择性α1和α2肾上腺素能受体拮抗剂哌唑嗪和育亨宾,对血管紧张素诱导的迷走神经反射性心动过缓的相互作用。可乐定(脑池内注射1 - 10微克)对血管紧张素的升压反应影响很小,仅略微增加了峰值,但显著延长了反射性心动过缓的持续时间。哌唑嗪和育亨宾(脑池内注射200微克任何一种拮抗剂)对血管紧张素引起的反射性心动过缓均无任何影响。育亨宾大大减弱了可乐定诱导的反应增强作用,但哌唑嗪没有作用。可乐定似乎通过刺激中枢α2肾上腺素能受体来增强迷走神经反射性心动过缓。