Passo S S, Thornborough J R, Rothballer A B
Can J Physiol Pharmacol. 1975 Jun;53(3):363-7. doi: 10.1139/y75-052.
Perfusion of the fourth cerebral ventricle with high-sodium artificial cerebrospinal fluid was found to result in an increase in urinary sodium excretion in anesthetized cats. The natriuresis was accompanied by an increase in blood pressure and glomerular filtration rate. However, in animals with the changes in blood pressure and glomerular filtration rate prevented by alpha adrenergic blockade (phenoxybenzamine), the increase in urinary sodium excretion persisted. the data suggest the presence of a neural mechanism in the vicinity of the fourth ventricle sensitive to cerebrospinal fluid sodium levels and capable of affecting urinary sodium excretion independent of changes in blood pressure or glomerular filtration rate. The possible role of the area postrema and adjacent medulla is considered.
研究发现，向麻醉猫的第四脑室灌注高钠人工脑脊液会导致尿钠排泄增加。利钠作用伴随着血压和肾小球滤过率的升高。然而，在通过α肾上腺素能阻断（酚苄明）防止血压和肾小球滤过率发生变化的动物中，尿钠排泄的增加仍然持续。这些数据表明，在第四脑室附近存在一种神经机制，该机制对脑脊液钠水平敏感，并且能够独立于血压或肾小球滤过率的变化而影响尿钠排泄。文中考虑了最后区和邻近延髓的可能作用。
