Fejes-Toth G, Naray-Fejes-Toth A, Frölich J C
J Pharmacol Exp Ther. 1983 Oct;227(1):215-9.
Although it is well established that chronic treatment with antidiuretic hormone increases renal prostaglandin (PG) excretion, the effects of short-term infusions are controversial. Therefore, in the present study the effect of acute administration of arginine vasopressin on urinary PG excretion was investigated in conscious Brattleboro rats and in water-diuresing Long-Evans rats. Water balance was kept constant during arginine vasopressin infusion. Arginine vasopressin caused a significant, dose-related and reversible increase in urinary PG excretion within 20 min in both models. Similar results were obtained during the infusion of 1-deamino-8-D-arginine vasopressin in the Brattleboro rat. Normalization of the hydropenia of Brattleboro rats by infusion of large amounts of hypotonic fluid failed to elevate urinary PG excretion. These results give no support to the hypothesis that the acute enhancement of urinary PG excretion by vasopressin is mediated through either vasoconstriction or volume retention or induction of cyclooxygenase, but rather they indicate that antidiuretic hormone can increase renal PG synthesis through a more direct mechanism in vivo.
尽管长期使用抗利尿激素会增加肾脏前列腺素（PG）排泄这一点已得到充分证实，但短期输注的效果仍存在争议。因此，在本研究中，我们在清醒的布拉特洛维大鼠和处于水利尿状态的朗-埃文斯大鼠中研究了急性给予精氨酸加压素对尿PG排泄的影响。在输注精氨酸加压素期间，水的平衡保持恒定。在两种模型中，精氨酸加压素均在20分钟内引起尿PG排泄显著、剂量相关且可逆的增加。在布拉特洛维大鼠中输注1-去氨基-8-D-精氨酸加压素期间也获得了类似结果。通过输注大量低渗液使布拉特洛维大鼠的缺水状态恢复正常并未能提高尿PG排泄。这些结果不支持以下假说，即加压素对尿PG排泄的急性增强作用是通过血管收缩、容量潴留或环氧化酶诱导介导的，相反，它们表明抗利尿激素可通过体内更直接的机制增加肾脏PG合成。
