Agnoli G C, Cacciari M, Cariani A
Minerva Med. 1975 Mar 3;66(16):729-58.
Renal, glomerular and tubular, factors responsible for the volume control of extracellular liquid were examined. The part played by angiotensin II in mediating the compensation of this liquid losses was studied in patients with spontaneous polyuria due to diencephalo-posthypophyseal diabetes insipidus or psychogenic polydipsia and healthy subjects with induced hypotonic polyuria. It was noted that: 1) acute expansion elicited a natriuretic response and increased distal sodium load, due to an increase in filtrate and relative inhibition of proximal reabsorption, or proximal inhibition if the filtrate was unchanged. The efficiency of distal sodium transport was often unchanged. 2) Return to sodium balance parity during prolonged expansion of volume, was accomplished by varying renal means, in accordance with the experimental model employed. Distal reabsorption was essentially depressed during prolonged saline load (secondary hypoaldosteronism). When protracted mineralcorticoid treatment was used, however, distal reabsorption was high, even in the escape stage, and its saturation required marked augmentation of the sodium load reaching the distal tubules. 3) Depletion of volume caused by protracted natriuretic treatment in spontaneous polyuria reduced both diuresis and sodium excretion. This resistance to the natriuretic effect of the drug followed intrarenal compensation that reduced the distal sodium load and encouraged reabsorption in some distal sites (secondary hyperaldosteronism). 4) Infusion of angiotensin II in sub- or pauci-pressor doses causes an isosmotic sodium saving, since it reduced the glomerular filtrate and increases the fraction of filtrate reabsorbed by the proximal tubules; the tubular effect is likely secondary to increased vascular, especially postglomerular resistance. In the healthy subject, angiotensin II leads to antidiuresis referable, on account of its intensity and longer time cycle, to ADH release angiotensin-dependent.
研究了肾脏、肾小球和肾小管中负责细胞外液容量控制的因素。在患有间脑 - 垂体后叶性尿崩症或精神性多饮导致的自发性多尿的患者以及诱导性低渗性多尿的健康受试者中，研究了血管紧张素II在介导这种液体丢失补偿中的作用。结果发现：1）急性扩容引发利钠反应并增加远端钠负荷，这是由于滤液增加和近端重吸收相对抑制所致，若滤液不变则是近端抑制。远端钠转运效率通常不变。2）在长时间扩容期间恢复钠平衡对等，是通过根据所采用的实验模型改变肾脏机制来实现的。在长时间盐水负荷期间（继发性醛固酮减少症），远端重吸收基本受到抑制。然而，当使用长时间的盐皮质激素治疗时，即使在逃逸阶段远端重吸收也很高，并且其饱和需要显著增加到达远端小管的钠负荷。3）在自发性多尿中，长时间利钠治疗导致的容量耗竭会降低尿量和钠排泄。对药物利钠作用的这种抵抗遵循肾内补偿，肾内补偿减少了远端钠负荷并促进了某些远端部位的重吸收（继发性醛固酮增多症）。4）输注亚升压或低升压剂量的血管紧张素II会导致等渗性钠潴留，因为它会减少肾小球滤过率并增加近端小管重吸收的滤液比例；肾小管效应可能继发于血管阻力增加，尤其是肾小球后阻力增加。在健康受试者中，由于血管紧张素II的强度和较长的时间周期，它会导致抗利尿作用，这归因于血管紧张素依赖性抗利尿激素的释放。
