Pierce E T, Grekin R J, Mouw D R
Am J Physiol. 1984 Jan;246(1 Pt 2):F32-8. doi: 10.1152/ajprenal.1984.246.1.F32.
Ventriculocisternal perfusion (VCP) of artificial cerebrospinal fluid (CSF) was performed in pentobarbital-anesthetized dogs. Renal function was studied in protocols consisting of a 1-h experimental period in which the animals received either CSF with an elevated sodium concentration (300 mM, high Na) via VCP or antidiuretic hormone (ADH) intravenously, bracketed by 1-h control and recovery periods. High Na VCP caused an increase in plasma ADH measured by radioimmunoassay (to 176% of control) that coincided with a natriuresis (to 180% of control). In a second set of experiments, these changes in endogenous ADH were mimicked experimentally with intravenous infusions of synthetic ADH in animals receiving continuous VCP with normal sodium artificial CSF. The dose-response relationship between log ADH and urinary sodium excretion for the intravenous ADH experiments was not different from the relationship for those experiments in which ADH was elevated as a consequence of high Na VCP. These results suggest that ADH causes part, if not all, the natriuresis induced by high Na VCP.
在戊巴比妥麻醉的犬身上进行人工脑脊液（CSF）的脑室池灌注（VCP）。通过实验方案研究肾功能，该方案包括一个1小时的实验期，在此期间动物通过VCP接受钠浓度升高（300 mM，高钠）的CSF或静脉注射抗利尿激素（ADH），前后各有1小时的对照期和恢复期。高钠VCP导致通过放射免疫测定法测得的血浆ADH增加（升至对照值的176%），同时伴有尿钠增多（升至对照值的180%）。在第二组实验中，在接受正常钠人工脑脊液持续VCP的动物中，通过静脉输注合成ADH模拟内源性ADH的这些变化。静脉注射ADH实验中log ADH与尿钠排泄之间的剂量反应关系与高钠VCP导致ADH升高的实验中的关系并无不同。这些结果表明，ADH至少部分地导致了高钠VCP诱导的尿钠增多。
