Hypertension: a disease of abnormal circulatory control.
Hypertension: a disease of abnormal circulatory control.
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高血压：一种循环控制异常的疾病。
作者：
A. C. Guyton;Allen W. Cowley;Thomas G. Coleman;J. DeClue;R. A. Norman;R. Manning
人们普遍认为，一些快速作用的压力控制机制，如压力感受器反馈机制和肾素血管紧张素机制也是长期动脉压控制的主要决定因素。但是，最近的理论分析，大量的实验和临床证据的支持下，已经表明，长期的压力水平的主要控制器是一个肾-体液体积反馈机制的压力控制。这一机制的运作简单如下：动脉压的升高导致肾脏排泄的尿液量显著增加。这反过来又会降低体液水平，最终使动脉压降至正常水平。然而，短期动脉压控制机制在急性实验中掩盖了这一机制。因此，直到最近，急性实验都未能证明流体机制的极端重要性和效力。用于压力控制的肾-体液体积机构是积分控制型的反馈控制系统，在适当的条件下，该反馈控制系统具有使动脉压返回到其参考压力水平的无限能力。该参考压力水平由两个主要因素确定：（1）尿量负荷;和（2）将动脉压与尿量负荷相关联的肾功能曲线。其中第二个通常更为重要。因此，肾脏在长期动脉压调节和高血压中起着几乎不可克服的作用。非肾性高血压异常在理论上和实验上都可以通过改变肾功能或液体摄入引起高血压。研究表明，肾中最负责控制动脉压的部分是肾小管前节段：传入小动脉和肾小球膜。因此，可以预测，大多数类型的高血压机制必须以这样或那样的方式由肾脏的一个前小管元件的原发性或继发性功能异常引起。
There is a widespread belief that some of the rapidly acting pressure control mechanisms such as the baroreceptor feedback mechanism and the reninangiotensin mechanism are also the primary determinant factors for longterm arterial pressure control. But recent theoretical analyses, supported by great amounts of experimental and clinical evidence, have shown that the primary controller of the longterm pressure level is a renal-body fluid volume feedback mechanism for pressure control. This mechanism operates simply as follows: an increase in arterial pressure causes the kidneys to excrete markedly increased quantities of urine. This, in turn, decreases the level of body fluids and eventually decreases the arterial pressure toward normal. However, the short-term arterial pressure control mechanisms obscure this mechanism in acute experiments. Therefore, acute experiments have, until recently, failed to demonstrate the extreme importance and potency of the fluid mechanism. The renal-body fluid volume mechanism for pressure control is a feedback control system of the integral control type that, under appropriate conditions, has infinite capability to return the arterial pressure to its reference pressure level. This reference pressure level is determined by two primary factors: (1) the urinary volume load; and (2) the renal function curve that relates arterial pressure to the urinary volume load. The second of these is usually by far the more important. Therefore, the kidneys play an almost insuperable role in longterm arterial pressure regulation and in hypertension. Nonrenal hypertensive abnormalities can be shown both theoretically and experimentally to cause hypertension by altering either kidney function or fluid intake. Studies indicate that the portions of the kidney most responsible for arterial pressure control are the pretubular segments: the afferent arterioles and the glomerular membrane. Therefore, one can predict that most types of hypertension mechanisms must in one way or another result from primary or secondary abnormal function of one of the pretubular elements of the kidney.