Ajayi A A, Reid J L
University Department of Materia Medica, Stobhill General Hospital, Glasgow, Scotland.
Int J Clin Pharmacol Res. 1988;8(5):327-33.
The renin-angiotensin system and the sympathetic nervous system are important control mechanisms in blood pressure regulation. A large body of in vitro and in vivo animal data indicate that angiotensin II regulates noradrenaline release and modifies sympathetic reflexes, although the physiological relevance of these to normal man remains unclear. It is established, however, that increasing age and hypertension independently modify autonomic responses in man. The hypothesis was therefore examined that angiotensin II exerts a pre-junctional effect on noradrenaline release and sympathetic cardiovascular function, in the elderly and in patients with essential hypertension. Inhibition of angiotensin-converting enzyme with enalapril and cilazapril, after short-term administration at doses sufficient to reduce circulating angiotensin II concentrations, did not alter sympathetically mediated orthostatic test, Valsalva's manoeuvre and cold pressor test, in young or elderly normotensives. Similarly, but in a separate study, the pressor, chronotropic and sympathoadrenal response to submaximal dynamic exercise were unchanged, following short-term converting enzyme inhibition in normal persons and essential hypertensive patients. These findings do not support a role for angiotensin II in presynaptic facilitation or post-junctional potentiation of noradrenergic transmission. It is proposed that the renin-angiotensin system exerts an independent, rather than a regulatory influence on sympathetic function in blood pressure control, in normal and hypertensive man.
肾素-血管紧张素系统和交感神经系统是血压调节中的重要控制机制。大量体外和体内动物数据表明，血管紧张素II调节去甲肾上腺素释放并改变交感反射，尽管其与正常人类的生理相关性仍不清楚。然而，已证实年龄增长和高血压会独立改变人类的自主反应。因此，研究了血管紧张素II对老年人和原发性高血压患者去甲肾上腺素释放和交感心血管功能是否具有节前效应的假设。在短期给予足以降低循环血管紧张素II浓度的剂量的依那普利和西拉普利抑制血管紧张素转换酶后，年轻或老年血压正常者的交感神经介导的直立试验、瓦尔萨尔瓦动作和冷加压试验均未改变。同样，但在另一项研究中，正常人和原发性高血压患者在短期抑制转换酶后，对次最大动态运动的升压、变时和交感肾上腺反应未发生变化。这些发现不支持血管紧张素II在去甲肾上腺素能传递的突触前促进或节后增强中起作用。有人提出，在正常人和高血压患者中，肾素-血管紧张素系统在血压控制中对交感功能发挥独立而非调节作用。
