Thromboxane A2 in the paraventricular hypothalamic nucleus mediates glucoprivation-induced adrenomedullary outflow.
Thromboxane A2 in the paraventricular hypothalamic nucleus mediates glucoprivation-induced adrenomedullary outflow.
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下丘脑室旁核中的血栓素 A2 介导葡萄糖缺乏引起的肾上腺髓质流出。
DOI：
10.1016/j.ejphar.2020.173034
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发表时间：
2020
期刊：
影响因子：
--
通讯作者：
Okada S.
中科院分区：
文献类型：
--
作者：
Tachi M;Yamaguchi N;Okada S.
葡萄糖缺乏刺激快速交感神经反应以释放和/或分泌儿茶酚胺到血流中。然而，涉及室旁下丘脑核（PVN）中肾上腺素受体和前列腺素类产生的中枢调节机制仍未解决，这些机制是葡萄糖缺乏诱导的血浆儿茶酚胺升高的原因。在本研究中，我们旨在阐明葡萄糖缺乏诱导的投射至PVN的去甲肾上腺素能神经元的激活是否可诱导PVN中的α和/或β肾上腺素能受体激活和前列腺素类物质产生，从而升高血浆儿茶酚胺水平。我们研究了α-和β-肾上腺素能受体拮抗剂、环氧合酶抑制剂、血栓素A合成酶抑制剂和前列腺素E 2亚型EP 3受体拮抗剂对静脉注射2-脱氧-D-葡萄糖（2-DG）诱导的室旁核去甲肾上腺素和血浆儿茶酚胺水平升高的影响。此外，我们研究了静脉注射2-DG是否可以增加PVN微透析液中的前列腺素水平。脑室内（i. c. v.）用酚妥拉明（一种非选择性α-肾上腺素能受体拮抗剂）预处理抑制2-DG诱导的血浆肾上腺素水平的升高，而用普萘洛尔（一种非选择性β-肾上腺素能受体拮抗剂）i. c. v.预处理抑制2-DG诱导的血浆去甲肾上腺素水平的升高。静脉注射吲哚美辛（一种环氧合酶抑制剂）和呋喃丙酯（一种血栓素合酶抑制剂）预处理减弱了2-DG诱导的去甲肾上腺素和肾上腺素水平升高。此外，2-DG给药升高了PVN微透析液中血栓烷A2的代谢产物血栓烷B2水平。我们的研究结果表明，葡萄糖缺乏诱导的α-和β-肾上腺素能受体的激活，包括PVN，然后在PVN血栓素A2的生产，这是必不可少的2-DG诱导的血浆肾上腺素和去甲肾上腺素水平的升高。
Glucoprivation stimulates a rapid sympathetic response to release and/or secrete catecholamines into the bloodstream. However, the central regulatory mechanisms involving adrenoceptors and prostanoids production in the paraventricular hypothalamic nucleus (PVN) that are responsible for the glucoprivation-induced elevation of plasma catecholamines are still unresolved. In this study, we aimed to clarify whether glucoprivation-induced activation of noradrenergic neurons projecting to the PVN can induce α- and/or β-adrenergic receptor activation and prostanoids production in the PVN to elevate plasma catecholamine levels. We examined the effects of α- and β-adrenergic receptor antagonists, a cyclooxygenase inhibitor, a thromboxane A synthase inhibitor, and a PGE2subtype EP3receptor antagonist on intravenously administered 2-deoxy-D-glucose (2-DG)-induced elevation of noradrenaline in the PVN and plasma levels of catecholamine in freely moving rats. In addition, we examined whether intravenously administered 2-DG can increase prostanoids levels in the PVN microdialysates. Intracerebroventricular (i.c.v.) pretreatment with phentolamine (a non-selective α-adrenergic receptor antagonist) suppressed the 2-DG-induced increase in the plasma level of adrenaline, whereas i.c.v. pretreatment with propranolol (a non-selective β-adrenergic receptor antagonist) suppressed the 2-DG-induced elevation of the plasma level of noradrenaline. I.c.v. pretreatment with indomethacin (a cyclooxygenase inhibitor) and furegrelate (a thromboxane synthase inhibitor) attenuated the 2-DG-induced elevations of both noradrenaline and adrenaline levels. Furthermore, 2-DG administration elevated the thromboxane B2level, a metabolite of thromboxane A2in PVN microdialysates. Our results suggest that glucoprivation-induced activation of α- and β-adrenergic receptor in the brain including the PVN and then thromboxane A2production in the PVN, which are essential for the 2-DG-induced elevations of both plasma adrenaline and noradrenaline levels.
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