Kanashkina T A, Kuznetsova A A, Shakhmatova E I, Natochin Iu V
Ross Fiziol Zh Im I M Sechenova. 2006 Oct;92(10):1228-38.
In experiments on non-anesthetized rats with administration into stomach of water (5 ml/100 g body mass) direct correlation has been found between an increase of diuresis and excretion of solute free water (r = 0.98, p < 0.01), while after injection to these animals of 5 x 10(-11) M arginine-vasotocin - between an increase of diuresis and simultaneous rise reabsorption of solute free water (r = 0.8, p < 0.01). The rise of diuresis after the vasotocin injection is due to inhibition of sodium re- absorption, with the solute excretion fraction increasing from 2.6 +/- 0.2 % to 11.9 +/- 1.2, p < 0.001. A similar physiological paradox - an increase of diuresis with the simultaneous increase of reabsorption of solute free water - has been revealed at night hours in children with tendency for nocturnal enuresis (r = 0.64, p < 0.01). Mechanism responsible for this phenomenon consists in a rise of diuresis due to a decrease of sodium ion reabsorption in the ascending Henle loop limb. A problem is discussed of the homeostatic significance of a decrease of sodium reabsorption combined with an increase of solute-free water reabsorption; it is suggested that this phenomenon is based on a redistribution of reabsorption inside the nephron - a decrease of ion and water reabsorption in the initial parts of the nephron distal segment and an increase of solute free water reabsorption with the antidiuretic hormone-stimulated high osmotic permeability of terminal parts of renal tubules. An intraperitoneal injection of V1-anatagonist (OPC-21268) decreased the natriuretic component of response to arginine-vasotocin, while injection of V2-antagonist (OPC-31260) eliminated the antidiuretic component.
在对未麻醉大鼠进行的实验中，向胃内注入水（5毫升/100克体重）后，发现利尿增加与无溶质水排泄之间存在直接相关性（r = 0.98，p < 0.01），而向这些动物注射5×10⁻¹¹ M精氨酸 - 血管升压素后，利尿增加与无溶质水重吸收同时增加之间存在相关性（r = 0.8，p < 0.01）。注射血管升压素后利尿增加是由于钠重吸收受到抑制，溶质排泄分数从2.6±0.2%增加到11.9±1.2，p < 0.001。在有夜间遗尿倾向的儿童中，夜间也发现了类似的生理悖论——利尿增加同时无溶质水重吸收增加（r = 0.64，p < 0.01）。这种现象的机制在于，由于亨利氏袢升支粗段钠离子重吸收减少导致利尿增加。讨论了钠重吸收减少与无溶质水重吸收增加的稳态意义问题；有人提出，这种现象基于肾单位内重吸收的重新分布——肾单位远曲段起始部分离子和水重吸收减少，以及抗利尿激素刺激肾小管末端部分高渗透通透性导致无溶质水重吸收增加。腹腔注射V1拮抗剂（OPC - 21268）可降低对精氨酸 - 血管升压素反应的利钠成分，而注射V2拮抗剂（OPC - 31260）可消除抗利尿成分。
