Interaction between sympathetic and renin-angiotensin system.
Interaction between sympathetic and renin-angiotensin system.
复制标题
交感神经和肾素-血管紧张素系统之间的相互作用。
DOI：
10.1097/00004872-198412000-00002
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发表时间：
1984
影响因子：
4.9
通讯作者：
Wong,PC
中科院分区：
文献类型：
--
作者：
Zimmerman,BG;Sybertz,EJ;Wong,PC
交感神经系统（SNS）和肾素-血管紧张素系统（RAS）在基础和病理生理条件下独立或联合参与心血管功能调节的程度尚不清楚。许多研究都是在麻醉的手术应激动物上进行的，而不是在放松状态下的清醒动物上进行的，研究了它们在维持血压、支持心脏功能和基础条件下血流分布方面各自的作用。然而，有足够的证据来自清醒动物和人类受试者的实验，表明SNS对基础条件下的血压和局部血管阻力有滋补作用。神经节阻滞剂和α-肾上腺素能阻滞剂在清醒的实验动物和卧位人体中可适度降低血压||1-5]，表明在静息条件下存在显著的交感血管张力。RAS对基础状态下血压的紧张性影响可能不如SNS重要，但似乎仍然存在。这一声明是基于清醒的狗和人在给予血管紧张素转换酶（ACE）抑制剂后血压降低的发现[6-8]，尽管在一项研究中没有发现这种作用[9]。然而，毫无疑问，SNS和RAS在各种病理生理状态下都被强烈激活[10]，例如出血，肾血管性高血压，充血性心力衰竭和在盐和水限制期间。可以问的一个问题是SNS和RAS是独立地还是协同地发挥作用以实现这种稳态作用。近年来，已经了解了SNS、RAS和精氨酸加压素在支持动脉血压中的各自作用。通过特异性阻断剂，许多研究者已经剖析了这些心血管系统重要调节剂的个体作用[11-16]。我们的具体目标是研究可能的方式，其中两个监管系统，SNS和RAS，互动。加压素对循环的激素和可能的神经体液影响的考虑超出了本讨论的范围。读者可以参考最近关于这个问题的几篇评论||[17-20]我们将这些系统之间的相互作用描述如下，SNS或RAS可以被血压变化反射性地激活以实现支持性心血管作用，而另一个将发挥储备能力。如果在激活后，第一个系统功能受损或受阻，第二个系统将发挥作用。如果我们假设SNS起主要作用，并且这似乎是基础条件下的情况，则其消除导致RAS的激活。当然，也可能发生相反的事件，如在肾血管性高血压的急性期。在这种情况下，RAS在维持高血压状态方面占据主导地位，在其去除后，SNS将承担主要的血压支持作用。在这样一种制度下，一个制度对另一个制度起调节作用的机会很少或根本没有。第二种可能的事件顺序是当血压受损时同时刺激SNS和RAS。这可能发生在由出血引起的重度水肿反应期间，
It is not well understood to what extent the sympathetic nervous system (SNS) and renin-angiotensin systems (RAS) participate either independently or conjointly in the regulation of cardiovascular function under basal and pathophysiological conditions. Many investigations examining their respective roles in blood pressure maintenance, support of cardiac function and distri-bution of blood flow under basal conditions have been conducted on anaesthetized surgically stressed animals, and not in conscious animals in a relaxed state. Nevertheless, there is sufficient evidence derived from experiments in conscious animals and in human subjects to indicate that there is a tonic influence of the SNS On blood pressure and regional vascular resistance under basal conditions. Ganglionic and alpha-adrenergic blocking agents lower blood pressure to a moderate degree in conscious experimental animals and in the recumbent human|| 1-5] suggesting that there is significant sympathetic vascular tone under resting conditions. The tonic influence of the RAS on blood pressure in the basal state may be less important than that of the SNS, but still seems to be present. This statement is based on the finding of a decrease in blood pressure in the conscious dog and human after administration Of angiotensin converting-enzyme (ACE) inhibitors [6-8], although in one investigation no such effect was found [9] There is no question, however, that both the SNS and RAS are strongly activated in various pathophysiological states [10], eg haenorrhage, renovascular hypertension, congestive heart failure and during salt and water restriction. A question that can be asked is whether the SNS and RAS are brought into play independently or in concert to accomplish this homeostatic role, In recent years much has been learned of the respective roles of the SNS, RAS and arginine vasopressin in the support of arterial blood pressure. Through the of specific blocking agents numerous investigators have dissected the individual contributions of these important regulators of the cardivascular system [11-16]. Our specific aim is to examine possible ways in which two of these regulatory systems, the SNS and RAS, interact. A consideration of vasopressin's hormonal and possible neurohumoral influences on the circulation is beyond the scope of the present discussion. The reader is directed to several recent reviews on this subject|| 17-20] We picture the interaction between these systems as follows, Either the SNS or RAS could be reflexly activated by blood pressure changes to fulfill a supportive cardiovascular role, and the other would function in a reserve capacity. If after its activation, the first system were functionally impaired or blocked pharmacologically, the second would be brought into play. If we assume that the SNS serves the primary role, and this seems to be the case under basal conditions, its elimination leads to the activation of the RAS. Of COurSe, the opposite sequence of events might also occur, eg aS in the acute phase of renovascular hypertension. In this case the RAS predominates in the maintenance of the hypertensive state, and after its removal the SNS would then take on the primary blood pressure supportive role. Under Such a scheme there would be little or no opportunity for a modulating role of one system on the other. A second possible sequence of events is for the SNS and RAS to be stimulated concurrently when blood pressure is compromized. This could occur during a severe hypotensive response caused by haemorrhage or