Clough D P, Mulroy S C, Angell D, Hatton R
Clin Exp Hypertens A. 1983;5(7-8):1287-99. doi: 10.3109/10641968309048858.
In the pithed rat preparation captopril, enalapril, teprotide and saralasin given intravenously attenuated pressor responses to both spinal sympathetic nerve stimulation and exogenous noradrenaline, indicating that angiotensin has a potent adrenergic facilitating action. Bi-lateral nephrectomy abolished the effects of captopril on nerve stimulation but responses to noradrenaline were still inhibited following nephrectomy, indicating that part of the post-junctional actions of captopril might not be angiotensin dependent. Both phenylephrine and clonidine are also inhibited by captopril in the pithed rat. It is thus not clear whether captopril is interacting with post-junctional alpha 1- or alpha 2-adrenoceptors. Vasoconstrictor responses to nerve stimulation are greater in SHR than WKY and captopril is more effective at inhibiting responses in the SHR than it is in WKY. These interactions between captopril and the sympathetic nervous system could explain the effectiveness of ACE inhibitors as antihypertensive agents.
在脊髓麻醉大鼠制备实验中，静脉注射卡托普利、依那普利、替普罗肽和沙拉新可减弱对脊髓交感神经刺激和外源性去甲肾上腺素的升压反应，表明血管紧张素具有强大的肾上腺素能易化作用。双侧肾切除消除了卡托普利对神经刺激的作用，但肾切除后对去甲肾上腺素的反应仍受抑制，这表明卡托普利的部分节后作用可能不依赖于血管紧张素。在脊髓麻醉大鼠中，去氧肾上腺素和可乐定也受到卡托普利的抑制。因此，尚不清楚卡托普利是否与节后α1或α2肾上腺素能受体相互作用。自发性高血压大鼠（SHR）对神经刺激的血管收缩反应比WKY大鼠更大，并且卡托普利在抑制SHR的反应方面比在WKY大鼠中更有效。卡托普利与交感神经系统之间的这些相互作用可以解释血管紧张素转换酶抑制剂作为抗高血压药物的有效性。
