McKinley M J, Denton D A, Coghlan J P, Harvey R B, McDougall J G, Rundgren M, Scoggins B A, Weisinger R S
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Parkville, Australia.
Can J Physiol Pharmacol. 1987 Aug;65(8):1724-9. doi: 10.1139/y87-271.
Studies in sheep have shown that renal excretion of sodium may be under osmoregulatory control. When sheep become dehydrated, or are infused intravenously with hypertonic saline, they increase renal Na excretion in addition to secreting vasopressin and developing a thirst. These natriuretic, antidiuretic, and dipsogenic responses to dehydration and hypertonicity can be greatly reduced by lowering the cerebrospinal fluid NaCl concentration or by prior ablation of tissue in the anterior wall of the third ventricle. Lowering of cerebrospinal fluid NaCl concentration also prevents postprandial natriuresis which normally occurs in association with a postprandial increase in plasma Na concentration and tonicity. We propose that there is a cerebral osmoregulatory control of Na excretion which may interact with volume influences from the cardiovascular system to regulate renal Na output. The effector mechanism from brain to kidney mediating such cerebral control of Na excretion is probably hormonal.
对绵羊的研究表明，钠的肾脏排泄可能受渗透调节控制。当绵羊脱水时，或静脉输注高渗盐水时，它们除了分泌抗利尿激素和产生口渴感外，还会增加肾脏钠排泄。通过降低脑脊液氯化钠浓度或预先切除第三脑室前壁组织，对脱水和高渗的这些利钠、抗利尿和致渴反应可大大降低。降低脑脊液氯化钠浓度还可防止通常与餐后血浆钠浓度和渗透压升高相关的餐后利钠作用。我们提出，存在对钠排泄的脑渗透调节控制，其可能与来自心血管系统的容量影响相互作用，以调节肾脏钠输出。从大脑到肾脏介导这种钠排泄脑控制的效应机制可能是激素性的。
