Nicholls M G, Espiner E A, Miles K D, Zweifler A J, Julius S
Clin Endocrinol (Oxf). 1981 Nov;15(5):423-30. doi: 10.1111/j.1365-2265.1981.tb00684.x.
Animal experiments indicate that angiotensin II can, under some circumstances stimulate the sympathetic nervous system at a number of different sites. In order to determine whether such a relationship of the renin-angiotensin and sympathetic nervous system exists in man, we increased (by intravenous infusion), or decreased (by administering the oral converting enzyme inhibitor captopril) circulating angiotensin II levels and monitored plasma adrenaline and noradrenaline responses. Angiotensin II infusions did not increase plasma catechol-amines, and lowering of angiotensin II by captopril treatment in patients with severe hypertension or congestive heart failure failed to alter plasma adrenaline or nor-adrenaline levels. Whether physiological levels of angiotensin II are capable of interacting directly with the sympathetic nervous system in man remains to be demonstrated.
动物实验表明，在某些情况下，血管紧张素II可在多个不同部位刺激交感神经系统。为了确定肾素 - 血管紧张素与交感神经系统之间是否存在这样的关系，我们通过静脉输注提高或通过口服转换酶抑制剂卡托普利降低循环中的血管紧张素II水平，并监测血浆肾上腺素和去甲肾上腺素的反应。输注血管紧张素II并未增加血浆儿茶酚胺，在重度高血压或充血性心力衰竭患者中，用卡托普利治疗降低血管紧张素II水平也未能改变血浆肾上腺素或去甲肾上腺素水平。血管紧张素II的生理水平是否能够直接与人的交感神经系统相互作用仍有待证实。
