Robinson A G, Roberts M M, Evron W A, Verbalis J G, Sherman T G
Department of Medicine, School of Medicine, University of Pittsburgh, Pennsylvania 15261.
J Clin Invest. 1990 Oct;86(4):1023-9. doi: 10.1172/JCI114804.
Hyponatremia due to inappropriate secretion of vasopressin is a common disorder in human pathophysiology, but vasopressin synthesis during hypoosmolality has not been investigated. We used a new method to quantitate synthesis of vasopressin in rats after 3, 7, and 14 d of hyponatremia induced by administering dDAVP (a vasopressin agonist) and a liquid diet. Vasopressin synthesis was completely turned off by 7 d. Vasopressin mRNA levels in the hypothalamus paralleled the reduction in synthesis and were reduced to levels of only 10-15% of the content in control rats. When hyponatremia was corrected by withdrawal of dDAVP, vasopressin mRNA slowly returned to normal over 7 d. The observation that vasopressin synthesis can be so completely turned off leads to several conclusions: under normal physiological conditions the neurohypophysis is chronically upregulated; there must be an osmotic threshold for initiation of vasopressin synthesis (and release); the large store of hormone in the posterior pituitary is essential for vasopressin to be available during times of decreased synthesis; and, finally, some nonosmolar stimulus for synthesis must be present during clinical disorders when vasopressin is secreted (and synthesized) despite hypoosmolality.
抗利尿激素分泌不当所致低钠血症是人类病理生理学中的常见病症，但低渗状态下抗利尿激素的合成尚未得到研究。我们采用一种新方法，对给予去氨加压素（一种抗利尿激素激动剂）和流食诱导大鼠低钠血症3天、7天及14天后的抗利尿激素合成进行定量分析。到第7天时，抗利尿激素合成完全停止。下丘脑抗利尿激素信使核糖核酸水平与合成减少情况平行，降至仅为对照大鼠含量的10% - 15%。当通过停用去氨加压素纠正低钠血症时，抗利尿激素信使核糖核酸在7天内缓慢恢复正常。抗利尿激素合成可如此完全停止这一观察结果引出了几个结论：在正常生理条件下，神经垂体长期处于上调状态；抗利尿激素合成（及释放）必定存在一个渗透阈值；垂体后叶中大量的激素储备对于合成减少时抗利尿激素的可利用性至关重要；最后，在临床病症中，当尽管处于低渗状态仍分泌（及合成）抗利尿激素时，必定存在某种非渗透刺激因素促使其合成。
