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心房利钠因子与电解质稳态的内分泌调节

Atrial natriuretic factor and the endocrine control of electrolyte homeostasis.

作者信息

Cogan E

机构信息

Department of Internal Medicine, Brugmann University Hospital, Brussels, Belgium.

出版信息

Acta Cardiol. 1991;46(3):377-84.

PMID:1833942
Abstract

The potent diuretic and natriuretic properties of atrial natriuretic factor (ANF) suggest that atrial hormones may participate to the regulation of salt and water excretion under physiological conditions. ANF, via the increase of its intracellular second messenger cGMP, has been recently shown to inhibit the apical sodium channel of the inner medullary collecting tubule (IMCD). In addition, ANF inhibits renin and aldosterone synthesis and antagonizes the antinatriuretic effects of angiotensin II. ANF may also contribute to the excretion of free water by inhibiting both the secretion of vasopressin and its antidiuretic action. ANF appears to play an important physiological role in sodium repleted states, or when the effective plasma volume is increased. On the contrary, when the effective plasma volume is decreased or in sodium depleted states, the natriuretic effect of both endogenous and exogenous ANF is severely blunted. That ANF-resistance may be related to the activation of the renin-angiotensin-aldosterone axis, increased circulating catecholamines, renal sympathetic nerve stimulation, changes in renal hemodynamics or increased degradation of ANF. All these factors could explain the lack of significant natriuretic effect of both endogenous and exogenous ANF in some pathological conditions such as heart failure or liver cirrhosis. ANF may also been concerned in water homeostasis. In addition to the well-known osmoregulatory pathways of water metabolism, we recently found that ANF could be involved in the volume adjustment to acute water intake in normal man.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

心房利钠因子(ANF)强大的利尿和利钠特性表明,心房激素可能在生理条件下参与盐和水排泄的调节。最近研究表明,ANF通过增加其细胞内第二信使环磷酸鸟苷(cGMP),抑制髓质内层集合管(IMCD)的顶端钠通道。此外,ANF抑制肾素和醛固酮的合成,并拮抗血管紧张素II的抗利钠作用。ANF还可能通过抑制血管加压素的分泌及其抗利尿作用,促进自由水的排泄。在钠负荷增加状态或有效血浆容量增加时,ANF似乎发挥重要的生理作用。相反,当有效血浆容量减少或处于钠缺乏状态时,内源性和外源性ANF的利钠作用都会严重减弱。ANF抵抗可能与肾素 - 血管紧张素 - 醛固酮轴的激活、循环儿茶酚胺增加、肾交感神经刺激、肾血流动力学变化或ANF降解增加有关。所有这些因素都可以解释在某些病理状态如心力衰竭或肝硬化时,内源性和外源性ANF缺乏显著利钠作用的原因。ANF也可能与水稳态有关。除了众所周知的水代谢渗透调节途径外,我们最近发现ANF可能参与正常人对急性水摄入的容量调节。(摘要截选至250字)

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