Yamamoto M, Share L, Shade R E
Neuroendocrinology. 1978;25(3):166-73. doi: 10.1159/000122738.
In anesthetized dogs, perfusion of the cerebral ventricles with indomethacin (IM), an inhibitor of prostaglandin biosynthesis, at rates of 1.9 or 7.6 microgram/min was without effect on the plasma ADH concentration. Ventriculo-cisternal perfusion with angiotensin II (AII; 19 ng/min) resulted in a 3-fold increase in the plasma ADH concentration within 45 min. When AII and IM were perfused together, the plasma ADH concentration increased only 2-fold, a response which was significantly lower than that obtained with AII alone. Thus, the ability of central AII to stimulate ADH release may depend, at least in part, upon the local release of prostaglandins.
在麻醉犬中,以1.9或7.6微克/分钟的速率向脑室灌注前列腺素生物合成抑制剂吲哚美辛(IM),对血浆抗利尿激素(ADH)浓度没有影响。以19纳克/分钟的速率向脑室-脑池灌注血管紧张素II(AII),45分钟内血浆ADH浓度增加了3倍。当AII和IM一起灌注时,血浆ADH浓度仅增加2倍,这一反应明显低于单独使用AII时的反应。因此,中枢AII刺激ADH释放的能力可能至少部分取决于前列腺素的局部释放。