Hamon G, Castillon A, Gaignault J C, Worcel M
Arch Int Pharmacodyn Ther. 1985 Jul;276(1):60-72.
The peripheral cardiovascular effects of tabernanthine tartrate have been studied in anaesthetized rats. Our results confirm that the bradycardic effect of tabernanthine is not inhibited by vagotomy, atropine or propranolol. On the contrary, bivagotomy, atropine treatment, as well as carotid artery occlusion, potentiate the bradycardic effect of tabernanthine. The same is true for its hypotensive action and can be explained by the suppression of a compensatory mechanism involving the central nervous system, the parasympathetic system and/or a baroreflex mechanism. In addition, domperidone and sulpiride, two dopaminolytic drugs, are able to potentiate the decrease in heart rate produced by tabernanthine. In pithed rat, tabernanthine 1 mg/kg, potentiates the increases in systolic blood pressure produced either by norepinephrine or serotonine; conversely the systolic blood pressure responses to angiotensin II are significantly inhibited by tabernanthine 1 mg/kg. Thus, tabernanthine appears to possess a complex cardiovascular mechanism of action, depending probably on a simultaneous stimulation of beta 2-vascular adrenoceptors and alteration of cellular movements of calcium. Part of the direct bradycardic effect, as well as the inhibition of the pressor responses of angiotensin II could be explained by a calcium antagonist action of the alcaloid.
已在麻醉大鼠中研究了酒石酸育亨宾的外周心血管效应。我们的结果证实，育亨宾的心动过缓效应不受迷走神经切断术、阿托品或普萘洛尔的抑制。相反，双侧迷走神经切断术、阿托品治疗以及颈动脉闭塞会增强育亨宾的心动过缓效应。其降压作用也是如此，这可以通过涉及中枢神经系统、副交感神经系统和/或压力反射机制的代偿机制的抑制来解释。此外，两种多巴胺能阻断药物多潘立酮和舒必利能够增强育亨宾引起的心率下降。在脊髓横断的大鼠中，1mg/kg的育亨宾会增强去甲肾上腺素或5-羟色胺引起的收缩压升高；相反，1mg/kg的育亨宾会显著抑制对血管紧张素II的收缩压反应。因此，育亨宾似乎具有复杂的心血管作用机制，可能取决于对β2-血管肾上腺素能受体的同时刺激以及钙的细胞运动改变。部分直接心动过缓效应以及对血管紧张素II升压反应的抑制可以用该生物碱的钙拮抗作用来解释。
