Hoffman W E, Weet J F, Phillips M I, Schmid P G
Neuroendocrinology. 1979;28(5):289-96. doi: 10.1159/000122874.
In unanesthetized water-loaded rats, intracerebroventricular (IVT) angiotensin II (AII) injections produce centrally mediated pressor effects and antidiuresis. Experiments were performed to evaluate the role of antidiuretic hormone (ADH) release versus neurogenic mechanisms in the antidiuretic responses to central AII median eminence lesions used to block ADH release abolish antidiuretic effects but only attenuated pressor responses to IVT AII infusions. Pretreatment with an intravenous infusion of ADH antibody had a similar effect. Central administration of AII in water and saline-loaded rats produced no change in effective renal plasma flow or glomerular filtration rate, Natriuretic and kaliuretic responses to IVT AII injections were similar to those observed to intravenous ADH infusions. These data are consistent with the suggestion that antidiuresis and osmotic excretion observed after IVT AII injections in the rats are the result of ADH release, and that neurogenic mechanisms play a major role in the blood pressure but not in the antidiuretic responses.
在未麻醉的水负荷大鼠中，脑室内（IVT）注射血管紧张素II（AII）会产生中枢介导的升压作用和抗利尿作用。进行实验以评估抗利尿激素（ADH）释放与神经源性机制在对中枢AII抗利尿反应中的作用。用于阻断ADH释放的正中隆起损伤消除了抗利尿作用，但仅减弱了对IVT AII输注的升压反应。静脉输注ADH抗体进行预处理具有类似的效果。在水负荷和盐负荷大鼠中中枢给予AII对有效肾血浆流量或肾小球滤过率没有影响，对IVT AII注射的利钠和利尿反应与静脉输注ADH时观察到的相似。这些数据与以下观点一致，即大鼠IVT AII注射后观察到的抗利尿和渗透排泄是ADH释放的结果，并且神经源性机制在血压调节中起主要作用，但在抗利尿反应中不起主要作用。
