Department of Physiology, National Defense Medical College, Saitama, Japan.
J Neuroendocrinol. 2009 Nov;21(11):921-34. doi: 10.1111/j.1365-2826.2009.01915.x. Epub 2009 Sep 1.
Peripherally secreted arginine vasopressin (AVP) plays a role in controlling body fluid homeostasis, and central endogenous AVP acts as a neurotransmitter or neuromodulator. The limbic system, which appears to exert an inhibitory effect on the endocrine hypothalamus, is also innervated by fibres that contain AVP. We examined whether central endogenous AVP is also involved in the control of body fluid homeostasis. To explore this possibility, we examined neuronal activity in the paraventricular nucleus of the hypothalamus (PVN), periventricular parts of the PVN and limbic brain areas, as well as AVP mRNA expression in the PVN and the peripheral secretion of AVP after central salt-loading in rats that had been pretreated i.c.v. with the AVP V(1) receptor antagonist OPC-21268. Neuronal activity in the PVN evaluated in terms of Fos-like immunoreactivity (FLI), especially in the parvocellular subdivisions, was suppressed. On the other hand, FLI was enhanced in the lateral septum, the bed nucleus of the stria terminalis and the anterior hypothalamic area. Similarly, AVP mRNA expression was enhanced in the magnocellular subnucleus of the PVN, despite the lack of a significant difference in the peripheral AVP level between OPC-21268- and vehicle-pretreated groups. We recorded renal sympathetic nerve activity (RSNA) as sympathetic nerve outflow during central salt-loading. The suppression of RSNA was significantly attenuated by i.c.v. pretreatment with OPC-21268. These results suggest that the suppression of RSNA during central salt-loading might be the result of a decrease in neuronal activity in the parvocellular subdivisions of the PVN via the inhibitory action of central endogenous AVP. The parvocellular and magnocellular neurones in the PVN might show different responses to central salt-loading to maintain body fluid homeostasis as a result of the modulatory role of central endogenous AVP.
外周分泌的精氨酸血管加压素（AVP）在控制体液稳态中发挥作用，而中枢内源性 AVP 作为神经递质或神经调质发挥作用。边缘系统似乎对内分泌下丘脑发挥抑制作用，也由包含 AVP 的纤维支配。我们研究了中枢内源性 AVP 是否也参与了体液稳态的控制。为了探索这种可能性，我们检查了下丘脑室旁核（PVN）、PVN 的室周部分和边缘脑区的神经元活动，以及经脑室预处理后接受中枢盐负荷的大鼠 PVN 中的 AVP mRNA 表达和 AVP 的外周分泌。用 AVP V1 受体拮抗剂 OPC-21268 预处理后，PVN 中的神经元活动（用 Fos 样免疫反应性（FLI）评估），特别是在小细胞亚区，受到抑制。另一方面，FLI 在外侧隔核、终纹床核和前下丘脑区增强。同样，尽管 OPC-21268 预处理组和载体预处理组之间外周 AVP 水平没有显著差异，但 PVN 的大细胞亚核中的 AVP mRNA 表达增强。在中枢盐负荷期间，我们记录了肾交感神经活动（RSNA）作为交感神经输出。脑室预处理用 OPC-21268 显著减轻了 RSNA 的抑制。这些结果表明，中枢盐负荷期间 RSNA 的抑制可能是由于中枢内源性 AVP 的抑制作用导致 PVN 的小细胞亚区神经元活动减少所致。PVN 的小细胞和大细胞神经元可能对中枢盐负荷表现出不同的反应，以维持体液稳态，这是由于中枢内源性 AVP 的调节作用。
