Aou S, Shiramine K, Ma J, Matsui H, Hori T
Department of Physiology, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Neurobiology (Bp). 1995;3(3-4):339-50.
Hypothalamic mechanisms of blood calcium homeostasis and their functional heterogeneity were investigated in rats. Electrical and chemical stimulation of the lateral hypothalamic area (LHA), the paraventricular nucleus (PVN) and the ventromedial nucleus of the hypothalamus (VMH) induced hypocalcemia. The hypocalcemic effect of PVN stimulation was suppressed by vagotomy of the thyroid/parathyroid branches, while that of LHA and VMH stimulation was eliminated by gastric vagotomy. Immobilization (IMB) stress elicited hypocalcemia through VMH-gastric vagal activation. Both IMB- and LHA stimulation-induced hypocalcemia was antagonized by muscarinic antagonist and histamine H2 blocker. The former was also blocked by alpha-blocker and gastrin release inhibitor, while the latter was antagonized by an beta-blocker. The results suggest that hypothalamic nuclei are involved in regulation of blood calcium homeostasis via the gastric or thyroid/parathyroid vagus. Muscarinic, histamine H2, adrenergic and gastrin receptors mediate the hypocalcemic effect of the hypothalamo-vagal activation depending on behavioral conditions and receptor subtypes.
在大鼠中研究了血钙稳态的下丘脑机制及其功能异质性。对下丘脑外侧区(LHA)、室旁核(PVN)和下丘脑腹内侧核(VMH)进行电刺激和化学刺激会诱发血钙过少。甲状腺/甲状旁腺分支的迷走神经切断术可抑制PVN刺激的血钙过少效应,而胃迷走神经切断术可消除LHA和VMH刺激的血钙过少效应。固定(IMB)应激通过VMH-胃迷走神经激活引发血钙过少。IMB刺激和LHA刺激诱导的血钙过少均被毒蕈碱拮抗剂和组胺H2阻滞剂拮抗。前者也被α阻滞剂和胃泌素释放抑制剂阻断,而后者被β阻滞剂拮抗。结果表明,下丘脑核通过胃或甲状腺/甲状旁腺迷走神经参与血钙稳态的调节。毒蕈碱、组胺H2、肾上腺素能和胃泌素受体根据行为条件和受体亚型介导下丘脑-迷走神经激活的血钙过少效应。