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肾脏和血容量在动脉血压调节及高血压中的作用。

Roles of the kidneys and fluid volumes in arterial pressure regulation and hypertension.

作者信息

Guyton A C

机构信息

Department of Physiology and Biophysics, University Medical Center, Jackson, Mississippi 39216.

出版信息

Chin J Physiol. 1989;32(2):49-57.

PMID:2700554
Abstract

The goal of this paper has been to show that the renal-fluid volume mechanism for control of the arterial pressure is an extremely powerful one, so powerful that it is either impossible or almost impossible for the arterial pressure ever to be adjusted to any other value besides the level dictated by this mechanism. The reason for the extreme potency of this mechanism for pressure control is that it never stops working until the intake and output of salt and fluid volume come to an exact state of equilibration. This occurs where the salt and water intake line, as illustrated in Figure 3, crosses the renal function curve which expresses the relationship between arterial pressure and fluid output by the kidneys. Some of the factors that make this renal-fluid volume mechanism such an excellent pressure regulator are the following: First, once the baroreceptor mechanism for pressure control has adapted, the systemic arterial pressure is affected greatly by the levels of extracellular fluid volume and blood volume. Second, the blood flow autoregulation mechanism further enhances the effect of slight changes in fluid volume on pressure, increasing the effectiveness of the pressure control system at least five times additional. Third, the renin-angiotensin system also plays a major role in increasing the sensitivity of this pressure control system. When salt intake becomes very great, renal output of renin and subsequent formation of angiotensin both decrease drastically. This shifts the renal function curve back toward a lower pressure level, thus compensating for most of the increase in pressure that would otherwise occur as a result of the increased salt intake. Putting all the above factors together, one finds that very slight changes in the fluid volume level in the body can have drastic effects on pressure. And, conversely, very slight changes in arterial pressure above or below the normal level can initiate large changes in urinary output of salt and water, thus rapidly returning the pressure back to that level at which intake and output of water and salt are in balance.

摘要

本文的目的是表明,肾液量机制对动脉血压的控制是一种极其强大的机制,强大到动脉血压几乎不可能被调整到该机制所决定的水平之外的任何其他值。这种压力控制机制极其有效的原因是,它在盐和液量的摄入与排出达到精确的平衡状态之前不会停止工作。这发生在盐和水摄入线(如图3所示)与表示动脉血压和肾脏液体排出之间关系的肾功能曲线相交处。使这种肾液量机制成为如此出色的压力调节器的一些因素如下:首先,一旦用于压力控制的压力感受器机制适应后,全身动脉血压会受到细胞外液量和血容量水平的极大影响。其次,血流自动调节机制进一步增强了液量微小变化对压力的影响,使压力控制系统的有效性至少额外提高了五倍。第三,肾素-血管紧张素系统在提高该压力控制系统的敏感性方面也起主要作用。当盐摄入量变得非常大时,肾素的肾脏输出以及随后血管紧张素的形成都会急剧下降。这会使肾功能曲线向较低压力水平回移,从而补偿了否则会因盐摄入量增加而出现的大部分压力升高。综合上述所有因素,人们发现体内液量水平的非常微小变化都可能对血压产生巨大影响。相反,动脉血压在正常水平之上或之下的非常微小变化都可能引发盐和水的尿量输出的大幅变化,从而迅速使血压恢复到水和盐的摄入与排出达到平衡的水平。

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