[房利钠因子]。

A. Mebazaa, D. Payen
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引用次数: 0

摘要

虽然心房利钠因子的研究早在30年前就开始了,但心房利钠因子(ANF)直到1981年才被发现。由于组织学和生理学上的争论,这种因素的存在已被怀疑多年。1956年,Kish在豚鼠的心房壁上发现了“致密颗粒”。Gauer和Henry只能通过暗示存在第三种激素因素来解释他们关于利尿和钠尿的一些实验结果,但既不是肾素-血管紧张素系统,也不是抗利尿激素。Hall等人首先认识到颗粒与水和钠代谢之间的联系。但正是德博尔德在1981年发表了这个关键的实验:给麻醉的大鼠注射右心房提取物,迅速引起了强烈和短暂的利尿和尿钠。ANF诞生了,同时,心脏作为内分泌腺的概念也诞生了。的确,ANF符合激素的严格定义。它具有以下特性:通过肾小球滤过分数的增加来尿钠和利尿,而肾血浆流量没有任何重大变化;对大动脉的直接血管扩张,对小动脉和静脉的影响很小。ANF分泌的刺激是机械的和药理学的,特别是目前麻醉师使用的药物。心房扩张是主要的机械刺激。心房经壁压力的增加总是伴随着ANF的释放,但这种效应对于腔内压力的增加不是恒定的。正是前一种压力梯度单独反映了右心房的容积,这是ANF分泌的机械刺激。心动过速,或者更准确地说,心房收缩率的增加,也会导致ANF的重要释放。心脏神经并不是必需的,正如对心脏移植患者的研究所证明的那样。只有少数药物被证明能真正刺激ANF的分泌。在大鼠中,吗啡有直接的分泌作用,而盐酸氯胺酮、二乙醚和水合氯醛则通过增加儿茶酚胺的释放而起作用。α、β肾上腺素能激动剂和钙激动剂的作用仍有争议。ANF具有利尿和血管扩张作用,与肾素-血管紧张素系统和抗利尿激素一起,在哺乳动物的血容量控制中起作用。然而,它有一个特殊的作用,因为它是一种快速释放激素:快速血管充盈导致ANF在不到1分钟内增加,与利尿平行增加。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
[Atrial natriuretic factor].
Although ANF research started 30 years ago, the atrial natriuretic factor (ANF) was only discovered recently (1981). The presence of such a factor has been suspected for many years because of histological and physiological arguments. In 1956, Kish found "dense granules" in the atrial walls of guinea pigs. Gauer and Henry could explain some of their experimental results on diuresis and natriuresis only by suggesting the presence of a third hormonal factor, but neither by the renin-angiotensin system, nor the anti-diuretic hormone. Hall et al. were the first to recognize a link between the granules and water and sodium metabolism. But it was De Bold who published the crucial experiment in 1981: injecting right atrial extracts to anaesthetized rats rapidly induced intense and transitory diuresis and natriuresis. ANF was born, and, at the same time, the concept of the heart as an endocrine gland. Indeed, ANF corresponds to the strict definition of a hormone. It has the following properties: natriuresis and diuresis via an increase in glomerular filtration fraction without any major changes in renal plasma flow; direct vasodilation of the large arteries with only few effects on small arterioles and veins. The stimuli for ANF secretion are mechanical and pharmacological, especially drugs currently used by anaesthetists. Atrial distension is the main mechanical stimulus. An increase in atrial transmural pressure is always followed by a release in ANF, but this effect is not constant for increases in intra-luminal pressure. It is the former pressure gradient alone that reflects the volume of the right atrium, the mechanical stimulus for ANF secretion. Tachycardia, or, more precisely, an increase in the atrial contraction rate, also leads to an important release of ANF. Cardiac nerves are not necessary for this, as demonstrated by studies in heart transplant patients. Only few pharmacological agents have been shown to really stimulate ANF secretion. In rats, morphine has a direct secretory effect, whereas ketamine hydrochloride, diethylether and chloral hydrate do so by increasing the release of catecholamines. The effects of alpha, beta adrenergic agonists and calcium agonists remain controversial. ANF, which has diuretic and vasodilator effects, plays a part, together with the renin-angiotensin system and the anti-diuretic hormone, in blood volume control in mammals. However, it has a special role to play, because it is a rapid release hormone: rapid vascular filling leads to an increase in ANF in less than 1 minute, with a parallel increase in diuresis.
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