Negoro H, Higuchi T, Tadokoro Y, Honda K
Department of Physiology, Fukui Medical School, Japan.
Jpn J Physiol. 1988;38(1):19-31. doi: 10.2170/jjphysiol.38.19.
In order to determine whether oxytocin release is controlled by an osmoreceptor mechanism identical with that for vasopressin release, the plasma oxytocin concentration and plasma osmolality were measured during intraatrial infusion and after intraventricular injection of various osmotic solutions in unanesthetized rats. Intraatrial infusion of 0.6 M NaCl Locke solution (L.S.) or 1.2 M mannitol L.S. elevated plasma oxytocin significantly, while 1.2 M urea L.S. caused only a small increase and isotonic L.S. did not change in plasma oxytocin. All hypertonic solutions produced significant and similar increases in the plasma osmolality. Plasma oxytocin was positively correlated with plasma osmolality in the animals infused with hypertonic NaCl or mannitol but not in the animals infused with hypertonic urea. The injection of 2 microliters of 0.6 M NaCl artificial cerebrospinal fluid (CSF) or 1.2 M mannitol CSF into the third ventricle caused a significant increase in plasma oxytocin immediately (5 min after injection) without changing plasma osmolality, while the intraventricular injection of 1.2 M urea CSF or isotonic CSF produced no significant change in plasma oxytocin. These results indicate that oxytocin release is controlled by osmoreceptors rather than Na receptors, that the adequate stimulus for the osmoreceptors is one which produces cellular dehydration and that the osmoreceptors are located in the brain region which is accessible to osmotic agents from both the outside and inside of the blood-brain barrier. Since the organum vasculosum of the lamina terminalis (OVLT) lacks a blood-brain barrier and is known to be involved in osmotic control of vasopressin release, a lesion was made in the anteroventral region of the third ventricle which encompasses the OVLT and the effect of hypertonic NaCl infusion on oxytocin release was examined. No significant increase in plasma oxytocin was observed after intraatrial infusion of 0.6 M NaCl L.S. in the lesioned rats. All of these findings lead to the conclusion that oxytocin release is under the control of osmoreceptors identical to those for vasopressin release.
为了确定催产素释放是否受与抗利尿激素释放相同的渗透压感受器机制控制，在未麻醉大鼠心房内输注以及脑室内注射各种渗透压溶液期间和之后，测量血浆催产素浓度和血浆渗透压。心房内输注0.6M NaCl洛克溶液（L.S.）或1.2M甘露醇L.S.可显著升高血浆催产素，而1.2M尿素L.S.仅引起小幅升高，等渗L.S.则不会改变血浆催产素。所有高渗溶液均使血浆渗透压显著且相似地升高。在输注高渗NaCl或甘露醇的动物中，血浆催产素与血浆渗透压呈正相关，但在输注高渗尿素的动物中并非如此。向第三脑室内注射2微升0.6M NaCl人工脑脊液（CSF）或1.2M甘露醇CSF可立即（注射后5分钟）显著增加血浆催产素，而不改变血浆渗透压，而脑室内注射1.2M尿素CSF或等渗CSF则不会使血浆催产素发生显著变化。这些结果表明，催产素释放受渗透压感受器而非钠感受器控制，渗透压感受器的适宜刺激是导致细胞脱水的刺激，且渗透压感受器位于血脑屏障内外的渗透剂均可到达的脑区。由于终板血管器（OVLT）缺乏血脑屏障且已知参与抗利尿激素释放的渗透压控制，于是在包含OVLT的第三脑室前腹侧区域制造损伤，并检查高渗NaCl输注对催产素释放的影响。在损伤大鼠中，心房内输注0.6M NaCl L.S.后未观察到血浆催产素显著增加。所有这些发现得出结论：催产素释放受与抗利尿激素释放相同的渗透压感受器控制。
