Yamaguchi K, Hama H, Watanabe K, Yamaya K
Department of Physiology, Niigata University School of Medicine, Japan.
Eur J Endocrinol. 1994 Dec;131(6):658-63. doi: 10.1530/eje.0.1310658.
The aim of the present study was to evaluate a role in vasopressin secretion of the catecholaminergic neurons, including the tuberohypophysial dopaminergic neurons situated in the arcuate hypothalamic nucleus. A neurotoxin, 6-hydroxydopamine (6 g/l), was injected locally into the arcuate nucleus and its effects on catecholamine levels of the hypothalamic tissue and the neurointermediate lobe, and on the plasma vasopressin concentrations before and during i.v. infusion (0.1 ml kg-1 min-1) of isotonic (0.15 mol/l) or hypertonic saline (2.5 mol/l), were examined in conscious rats. The infusion of hypertonic saline produced increases of plasma vasopressin 15 and 30 min later, accompanied by elevations of plasma osmolality, sodium, chloride and arterial pressure. The vasopressin response was potentiated markedly by the 6-hydroxydopamine injection performed 8 days before, which hardly affected the responses of the other variables. Histological examination indicated that the injection sites of 6-hydroxydopamine in those rats had been located in the area ranging from rostral to medial arcuate nucleus. The i.v. infusion of isotonic saline did not change plasma vasopressin, osmolality, sodium, chloride or arterial pressure, regardless of the presence or absence of pretreatment with 6-hydroxydopamine. It was confirmed that when 6-hydroxydopamine was injected into the arcuate nucleus region 8 days before, noradrenaline and adrenaline concentrations of the hypothalamic tissue containing the injection site were decreased remarkably, although we could not detect any significant alteration in the dopamine concentration of the hypothalamic tissue or the neurointermediate lobe. On the basis of these results, we concluded that catecholaminergic neurons in the arcuate nucleus may act to inhibit osmotic vasopressin secretion.
本研究的目的是评估儿茶酚胺能神经元(包括位于下丘脑弓状核的结节漏斗多巴胺能神经元)在血管加压素分泌中的作用。将神经毒素6-羟基多巴胺(6 g/l)局部注射到弓状核中,并检测其对下丘脑组织和神经中间叶中儿茶酚胺水平的影响,以及对清醒大鼠静脉输注(0.1 ml kg-1 min-1)等渗(0.15 mol/l)或高渗盐水(2.5 mol/l)之前及期间血浆血管加压素浓度的影响。输注高渗盐水15和30分钟后血浆血管加压素增加,同时伴有血浆渗透压、钠、氯和动脉压升高。8天前进行的6-羟基多巴胺注射显著增强了血管加压素反应,而这几乎不影响其他变量的反应。组织学检查表明,这些大鼠中6-羟基多巴胺的注射部位位于从弓状核嘴侧到内侧的区域。无论是否用6-羟基多巴胺预处理,静脉输注等渗盐水均未改变血浆血管加压素、渗透压、钠、氯或动脉压。证实当8天前将6-羟基多巴胺注射到弓状核区域时,含注射部位的下丘脑组织中去甲肾上腺素和肾上腺素浓度显著降低,尽管我们未检测到下丘脑组织或神经中间叶中多巴胺浓度有任何显著变化。基于这些结果,我们得出结论,弓状核中的儿茶酚胺能神经元可能起到抑制渗透性血管加压素分泌的作用。