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血管加压素在心血管控制中的作用:循环血管加压素的作用

Vasopressin in cardiovascular control: role of circulating vasopressin.

作者信息

Liard J F

出版信息

Clin Sci (Lond). 1984 Nov;67(5):473-81. doi: 10.1042/cs0670473.

Abstract

Vasopressin has been shown to elicit vasoconstriction in unanaesthetized animals at plasma concentrations similar to those associated with its renal antidiuretic effect. The vasconstrictor effects of vasopressin do not normally translate into pressor responses until relatively high plasma concentrations are reached. This appears to be related to very effective buffering by the baroreceptor reflex. In the absence of afferent signals from the baroreceptors (surgical denervation, but more importantly, low arterial pressure), the vasoconstriction elicited by vasopressin represents a significant part of the mechanisms that determine blood pressure. Vasopressin is clearly involved in the short-term control of blood pressure in situations such as haemorrhage, other volume-depleted states and dehydration. However, it is only one of several short-acting mechanisms which complement each other in the defence against hypotensive stresses. Under different conditions, the cardiovascular effects of vasopressin seem to have a component related to the central nervous system control of the circulation. Whether or not circulating vasopressin interacts with the newly described network of extrahypothalamic projections from the paraventricular nucleus is yet conjectural. However, the presence in the brain of vasopressin-containing pathways and of various types of receptors to vasopressin, as well as the existence of cardiovascular effects elicited by central administration of antidiuretic hormone, suggests a role for cerebral vasopressin in the control of autonomic function. Slightly elevated levels of vasopressin have been found in various forms of hypertension. Yet, the role of vasopressin, when present, may be more related to its antidiuretic than to its vasoconstrictor properties.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

血管加压素已被证明,在未麻醉动物中,当血浆浓度与产生肾脏抗利尿作用时的浓度相似时,会引起血管收缩。血管加压素的血管收缩作用通常在达到相对较高的血浆浓度时才会转化为血压升高反应。这似乎与压力感受器反射的非常有效的缓冲作用有关。在没有来自压力感受器的传入信号时(手术去神经支配,但更重要的是动脉压低),血管加压素引起的血管收缩是决定血压机制的重要组成部分。在出血、其他血容量减少状态和脱水等情况下,血管加压素显然参与血压的短期控制。然而,它只是几种相互补充以抵御低血压应激的短效机制之一。在不同条件下,血管加压素的心血管作用似乎有一个与中枢神经系统对循环的控制有关的成分。循环中的血管加压素是否与新描述的室旁核下丘脑外投射网络相互作用尚不确定。然而,大脑中存在含血管加压素的通路和各种类型的血管加压素受体,以及中枢给予抗利尿激素会引起心血管效应,这表明脑内血管加压素在自主功能控制中起作用。在各种形式的高血压中已发现血管加压素水平略有升高。然而,当血管加压素存在时,其作用可能与其抗利尿特性而非血管收缩特性更相关。(摘要截短于250字)

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