The interaction between vasopressin and oxytocin neurons after central salt loading

加压素和催产素神经元之间的相互作用。我们使用免疫组织化学双标记技术检测了中央盐负荷对抗利尿激素（AVP）和催产素（OT）神经元活性的影响。垂体后叶加压素V_1受体拮抗剂阻断内源性垂体后叶加压素后，下丘脑室旁核（PVN） Fos阳性神经元数除以AVP或OT神经元数计算神经元活性比升高。另一方面，视上核（SON）的比例相反地降低。SON中神经元活性的降低与全身OT水平的降低是一致的。中央盐负荷诱导的内源性抗利尿激素可能促进OT向外周循环的分泌。内源性抗利尿激素在心力衰竭模型中的作用被调节。采用结扎左冠状动脉法制备充血性心力衰竭（CHF）模型大鼠，术后恢复3周以上。两组均给予高渗生理盐水（HS: 0.67 M）。一组用加压素V_1受体拮抗剂预处理，另一组只用HS。我们将PVN分为四个区域进行评估，内侧（PVM），外侧（PVL），背内侧帽（PVDC）和整个PVN （e-PVN）。抗利尿激素V_1受体拮抗剂阻断内源性抗利尿激素后，正常大鼠PVDC神经元活性增强，而CHF组则相反，与单独给药的各组相比，其促进作用消失。在什么范围内压力反应在中央盐加载成为应力？在此之前，我们发现高浓度hs （1.0 M）可以使PVN和SON的神经元活动趋于平稳。然后，我们假设更大的压力反应可能会抑制神经元活动，正如之前报道的那样。虽然我们试图用硝普钠（SNP）从26.5±4.0 mmHg降至-3.4±3.8 mmHg来对抗1.0 M HS给药期间的升压反应，但PVN和SON的神经元活性变化受到了更大的抑制。建议将血压强行控制在正常范围内可能成为一种应激源。少

The interaction between vasopressin and oxytocin neurons.We examined the effect of central salt loading on the neuronal activity in both vasopressin (AVP) and oxytocin (OT) neurons using double labeling techniques of immunohistochemistry. After blocking the endogenous vasopressin with vasopressin V_1 receptors antagonist, the neuronal activity ratio, which was calculated by divided the number of Fos positive neurons with the number of AVP or OT neurons, increased in the paraventricular nucleus (PVN) of the hypothalamus. On the other hand, the ratio in the supraoptic nucleus (SON) was conversely decreased. This decreased neuronal activity in the SON was compatible with the decreased systemic OT levels. Endogenous vasopressin induced by central salt loading might facilitate the secretion of OT to the peripheral circulation.The role of endogenous vasopressin was modulated in the heart failure models.We made the congestive heart failure (CHF) model rats by ligating the left coronary artery … More and used them after more than three weeks recovery. Then, hypertonic saline (HS : 0.67 M) were administered centrally to two groups. One is pretreated with vasopressin V_1 receptors antagonist and the other is administered with HS only. We divided the PVN into four regions for evaluation, medial (PVM), lateral (PVL), dorsomedial cap (PVDC), and entire PVN (e-PVN). After blocking the endogenous vasopressin by vasopressin V_1 receptors antagonist, the neuronal activity in the PVDC was enhanced in the normal rats group, but conversely the facilitation was disappeared in the CHF group compared with each HS-administered alone group, respectively.By what range does the pressor response during central salt loading become stress?Previously, we showed that administration of high concentrated-HS (1.0 M) leveled off the neuronal activity in the PVN and SON. Then, we hypothesized that the greater pressor response might suppress the neuronal activity as previously reported. Although we tried to counter the pressor response during 1.0 M HS administration using sodium nitroprusside (SNP) from 26.5 ± 4.0 mmHg to -3.4 ± 3.8 mmHg, the neuronal activity in the PVN and SON changed more suppressed. It is suggested that to manipulate the blood pressure forcibly within normal range might become kind of stressor. Less