Superoxide anions mediate the effects of angiotensin (1-7) analog, alamandine, on blood pressure and sympathetic activity in the paraventricular nucleus
Superoxide anions mediate the effects of angiotensin (1-7) analog, alamandine, on blood pressure and sympathetic activity in the paraventricular nucleus
复制标题
超氧阴离子介导血管紧张素 (1-7) 类似物、阿拉曼定对室旁核血压和交感神经活动的影响
DOI：
10.1016/j.peptides.2019.170101
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发表时间：
2019-08-01
期刊：
影响因子：
3
通讯作者：
Kong, Xiangqing
中科院分区：
文献类型：
--
作者：
Gong, Juexiao;Shen, Yihui;Kong, Xiangqing
向下丘脑室旁核（PVN）微注射almanmanine可增加血压和增强交感神经活动。本研究的目的是确定超氧阴离子是否调节杏仁胺在PVN中的作用。记录麻醉后正常血压Wistar-Kyoto （WKY）大鼠和自发性高血压大鼠的平均动脉压（MAP）和肾交感神经活动（RSNA）。在WKY大鼠和SHRs中，向PVN中微量注射almanmanine均增加了MAP和RSNA，但在SHRs中增加的程度更大。这些作用被alamandine receptor （MrgD）拮抗剂D-Pro(7)- ang -(1-7)预处理阻断。超氧阴离子清除剂tempol和铁以及NADPH氧化酶抑制剂apocynin （APO）预处理也阻断了almanmanine对MAP和RSNA的影响。此外，在PVN中使用超氧化物歧化酶（SOD）抑制剂二乙基二硫代氨基甲酸（DETC）预处理可增强almanmanine诱导的MAP和RSNA的升高，在SHRs中观察到更大的反应。SHRs大鼠PVN超氧阴离子和NADPH氧化酶水平高于WKY大鼠。almanmanine处理增加了WKY和SHRs中超氧阴离子和NADPH氧化酶的水平，但对SHRs的影响更大。D-Pro(7)- ang -(1-7)预处理均可抑制almanmanine诱导的PVN升高。这些结果表明，在正常和高血压大鼠中，PVN中的超氧阴离子调节杏仁胺诱导的血压和交感神经活动的增加。阿拉曼胺增加NADPH氧化酶活性，诱导超氧阴离子产生，这是由阿拉曼胺受体介导的。
Microinjection of alamandine into the hypothalamic paraventricular nucleus (PVN) increased blood pressure and enhanced sympathetic activity. The aim of this study was to determine if superoxide anions modulate alamandine's effects in the PVN. Mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) were recorded in anaesthetized normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHRs). Microinjection of alamandine into the PVN increased MAP and RSNA in both WKY rats and SHRs, although to a greater extent in SHRs. These effects were blocked by pretreatment with an alamandine receptor (MrgD) antagonist D-Pro(7)-Ang-(1-7). Pretreatment with superoxide anion scavengers, tempol and tiron, and NADPH oxidase inhibitor apocynin (APO), also blocked the effects of alamandine on MAP and RSNA. In addition, pretreatment in the PVN with a superoxide dismutase (SOD) inhibitor diethyldithiocarbamic acid (DETC) potentiated the increases of MAP and RSNA induced by alamandine administration, with a greater response observed in SHRs. Superoxide anions and NADPH oxidase levels in the PVN were higher in SHRs than that in WKY rats. Alamandine treatment increased the levels of superoxide anions and NADPH oxidase in WKY and SHRs, however, with greater effect in SHRs. These alamandine-induced increases were inhibited by D-Pro(7)-Ang-(1-7) pretreatment in the PVN of both rats. These results demonstrate that superoxide anions in the PVN modulate alamandine-induced increases in blood pressure and sympathetic activity in both normotensive and hypertensive rats. Alamandine increases NADPH oxidase activity to induce superoxide anion production, which is mediated by the alamandine receptor.