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心脏对盐食欲的控制。

Cardiac control of salt appetite.

作者信息

Toth E, Stelfox J, Kaufman S

出版信息

Am J Physiol. 1987 May;252(5 Pt 2):R925-9. doi: 10.1152/ajpregu.1987.252.5.R925.

DOI:10.1152/ajpregu.1987.252.5.R925
PMID:3578557
Abstract

Inflation of a balloon for 2 h at the superior vena caval-right atrial junction of the rat reduced the salt intake of animals that had been sodium and water depleted by peritoneal dialysis with hyperoncotic colloid. After the balloons were deflated, the experimental group drank more than the control group so that the total sodium intake of the two groups was the same. Thus stimulated increased venous return to the heart attenuates salt appetite. Since this phenomenon might be secondary to a reflex reduction in plasma renin activity, the experiment was repeated using a model of salt appetite in which the renin-angiotensin system is known to be suppressed, namely the deoxycorticosterone acetate-treated rat. Salt intake was again significantly reduced by inflation of the right atrial balloon. It is concluded that pathways exist, independent of the renin-angiotensin system, whereby information obtained from the cardiac volume receptors regarding the state of filling of the vasculature may be used to regulate salt intake.

摘要

在大鼠上腔静脉 - 右心房交界处将气球充气2小时,可降低经高渗胶体腹膜透析导致钠和水缺失的动物的盐摄入量。气球放气后,实验组的饮水量超过对照组,使得两组的总钠摄入量相同。因此,这种刺激导致的静脉回心血量增加会减弱盐食欲。由于这种现象可能继发于血浆肾素活性的反射性降低,因此使用一种已知肾素 - 血管紧张素系统被抑制的盐食欲模型(即醋酸脱氧皮质酮处理的大鼠)重复了该实验。右心房气球充气再次显著降低了盐摄入量。得出的结论是,存在独立于肾素 - 血管紧张素系统的途径,通过这些途径,从心脏容量感受器获得的有关血管系统充盈状态的信息可用于调节盐摄入量。

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