Schalekamp M A, Man in't Veld A J, Wenting G J
J Hypertens. 1985 Apr;3(2):97-108. doi: 10.1097/00004872-198504000-00001.
The autoregulation theory of essential hypertension states that the characteristic haemodynamic derangement of this disease, i.e. increased vascular resistance, is a homeostatic response to abnormal sodium retention by the kidneys. The postulated relationship between arterial pressure and urinary sodium excretion is disturbed in such a way that a higher than normal pressure is required for sodium excretion to keep up with intake. This will initially expand plasma volume and raise cardiac output. However, hyperperfusion of the tissues will ultimately induce vasoconstriction, presumably by greater than normal wash-out of vasodilator metabolic products. Thus, cardiac output will be restored. Some elements of this theory are not supported by current evidence, but the key element, i.e. the assumption that increased vascular resistance is somehow dependent on abnormal renal sodium handling, is consistent with the following clinical observations: Arterial pressure and urinary sodium excretion are directly correlated over a wide range of pressures in patients with autonomic failure, both acutely during titling and chronically with changes in posture during a 24-h period. The failure to demonstrate pressure-natriuresis in normal subjects may therefore be related to the amplifying effect of the sympathetic nervous system on this mechanism, so that small changes in pressure are capable of inducing large changes in sodium excretion. The pressure-natriuresis curve in patients with autonomic failure is shifted to higher pressures by administration of aldosterone, which is consistent with an important role of renal sodium retention in mineralocorticoid hypertension. Measurements of total extracellular fluid volume, plasma volume/interstitial fluid volume ratio, transcapillary escape rate of serum albumin, cardiac output and arterial pressure at timed intervals during the development of hypertension, in patients exposed to mineralocorticoid excess, or during the reversal of hypertension in nephrectomized patients treated with ultrafiltration haemodialysis, revealed an association of increased total peripheral resistance with a reduced plasma volume/interstitial fluid volume ratio and an increased transcapillary escape rate of serum albumin. This association has also been observed in cross-sectional studies of patients with essential hypertension and suggests that part of the increase in resistance is located at a post-capillary level. It may be related to compression of collapsible venules and veins due to abnormally increased interstitial fluid pressure, not only in sodium-dependent secondary forms of hypertension but also in essential hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
原发性高血压的自动调节理论认为，该疾病的特征性血流动力学紊乱，即血管阻力增加，是对肾脏异常钠潴留的一种稳态反应。动脉血压与尿钠排泄之间的假定关系受到干扰，以至于需要高于正常的压力才能使钠排泄跟上摄入。这最初会使血浆量增加并提高心输出量。然而，组织的过度灌注最终会导致血管收缩，推测是由于血管舒张代谢产物的清除超过正常水平。因此，心输出量将恢复正常。该理论的某些要素目前尚无证据支持，但关键要素，即血管阻力增加在某种程度上依赖于肾脏钠处理异常这一假设，与以下临床观察结果一致：在自主神经功能衰竭患者中，无论是在体位倾斜时急性观察，还是在24小时内姿势改变时慢性观察，动脉血压和尿钠排泄在很宽的血压范围内直接相关。因此，在正常受试者中未能证明压力-利钠关系，可能与交感神经系统对该机制的放大作用有关，以至于压力的微小变化就能引起钠排泄的大幅变化。给予醛固酮会使自主神经功能衰竭患者的压力-利钠曲线向更高压力偏移，这与肾脏钠潴留在盐皮质激素性高血压中的重要作用一致。在高血压发展过程中、盐皮质激素过多的患者中或接受超滤血液透析治疗的肾切除患者高血压逆转过程中，定时测量总细胞外液量、血浆量/组织间液量比值、血清白蛋白的跨毛细血管逸出率、心输出量和动脉血压，结果显示总外周阻力增加与血浆量/组织间液量比值降低以及血清白蛋白的跨毛细血管逸出率增加有关。在原发性高血压患者的横断面研究中也观察到了这种关联，这表明部分阻力增加位于毛细血管后水平。这可能与间质液压力异常增加导致可塌陷小静脉和静脉受压有关，不仅在钠依赖性继发性高血压中如此，在原发性高血压中也是如此。（摘要截选至400字）
