The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1-12) and angiotensin II
The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1-12) and angiotensin II
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DOI：
10.1152/ajpheart.01144.2010
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发表时间：
2011-03-01
影响因子：
4.8
通讯作者：
Sapru, Hreday N.
中科院分区：
文献类型：
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作者：
Arakawa, Hideki;Chitravanshi, Vineet C.;Sapru, Hreday N.
Arakawa H, Chitravanshi VC, Sapru HN。下丘脑弓状核：血管紧张素-(1-12)和血管紧张素II心血管作用的新位点。[J]中国生物医学工程学报，2011,31(2):559 - 563。首次发表于2010年12月24日；doi: 10.1152 / ajpheart.01144.2010。下丘脑弓状核（ARCN）已被报道在心血管调节中发挥重要作用。有人推测，ARCN可能是血管紧张素（ANGs）作用于心血管的部位之一。实验采用聚氨酯麻醉、人工通气的成年雄性Wistar大鼠。显微注射n -甲基- d -天冬氨酸（NMDA; 10 mM）鉴定ARCN。微注射（50 nl） ANG-(1-12) （1 mM）到ARCN引起平均动脉压（MAP）、心率（HR）升高和更大的内脏神经活动（GSNA）。双侧迷走神经切开术可减轻对ANG-(1-12)的心动过速反应。微注射ANG II 1型受体（AT(1)R）拮抗剂可减弱ANG-(1-12)引起的心血管反应，而微注射ANG II 2型受体（AT(2)R）拮抗剂则不能减弱。联合抑制ARCN中ANG转换酶（ACE）和切酶可消除ANG-(1-12)诱导的反应。向ARCN内微量注射1mm的ANG II也能增加MAP和HR。微注射muscimol （1 mM）抑制ARCN可减轻静脉注射ANG-(1-12)和ANG II（各300 pmol/kg）时的加压反应和心动过速反应。结果表明：1)微注射ANG-(1-12)可引起MAP、HR和GSNA的升高；2) HR反应由交感神经和迷走神经共同介导；3)在ARCN介导的ANG-(1-12)诱导的应答中，AT(1)Rs，而不是AT(2)Rs；4)在ARCN中，ANG-(1-12)转化为ANG II需要ACE和切酶的共同作用；5) ARCN介导心血管对循环ANGs的反应。
Arakawa H, Chitravanshi VC, Sapru HN. The hypothalamic arcuate nucleus: a new site of cardiovascular action of angiotensin-(1-12) and angiotensin II. Am J Physiol Heart Circ Physiol 300: H951-H960, 2011. First published December 24, 2010; doi: 10.1152/ajpheart.01144.2010.-The hypothalamic arcuate nucleus (ARCN) has been reported to play a significant role in cardiovascular regulation. It has been hypothesized that the ARCN may be one of the sites of cardiovascular actions of angiotensins (ANGs). Experiments were carried out in urethane-anesthetized, artificially ventilated, adult male Wistar rats. The ARCN was identified by microinjections of N-methyl-D-aspartic acid (NMDA; 10 mM). Microinjections (50 nl) of ANG-(1-12) (1 mM) into the ARCN elicited increases in mean arterial pressure (MAP), heart rate (HR), and greater splanchnic nerve activity (GSNA). The tachycardic responses to ANG-(1-12) were attenuated by bilateral vagotomy. The cardiovascular responses elicited by ANG-(1-12) were attenuated by microinjections of ANG II type 1 receptor (AT(1)R) antagonists but not ANG type 2 receptor (AT(2)R) antagonist. Combined inhibition of ANG-converting enzyme (ACE) and chymase in the ARCN abolished ANG-(1-12)-induced responses. Microinjections of ANG II (1 mM) into the ARCN also increased MAP and HR. Inhibition of ARCN by microinjections of muscimol (1 mM) attenuated the pressor and tachycardic responses to intravenously administered ANG-(1-12) and ANG II (300 pmol/kg each). These results indicated that 1) microinjections of ANG-(1-12) into the ARCN elicited increases in MAP, HR, and GSNA; 2) HR responses were mediated via both sympathetic and vagus nerves; 3) AT(1)Rs, but not AT(2)Rs, in the ARCN mediated ANG-(1-12)induced responses; 4) both ACE and chymase were needed to convert ANG-(1-12) to ANG II in the ARCN; and 5) ARCN plays a role in mediating the cardiovascular responses to circulating ANGs.