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蓝斑诱导大鼠压力感受性反射抑制过程中室旁核的去甲肾上腺素能神经传递

Noradrenergic neurotransmission at PVN in locus ceruleus-induced baroreflex suppression in rats.

作者信息

Hwang K R, Chan S H, Chan J Y

机构信息

Department of Medical Research, Veterans General Hospital-Taipei, Taiwan, Republic of China.

出版信息

Am J Physiol. 1998 Apr;274(4):H1284-92. doi: 10.1152/ajpheart.1998.274.4.H1284.

DOI:10.1152/ajpheart.1998.274.4.H1284
PMID:9575933
Abstract

We investigated the role of ascending noradrenergic projections from the locus ceruleus (LC) to the paraventricular nucleus (PVN) of the hypothalamus in LC-induced suppression of the baroreceptor reflex (BRR) response in adult Sprague-Dawley rats maintained under pentobarbital anesthesia. On the basis of in vivo microdialysis and high-performance liquid chromatography-electrochemical detection, microinjection of L-glutamate (5 nmol) into the LC resulted in a site-specific increase in norepinephrine (NE) concentration in the dialysate collected from the parvocellular subnucleus of the PVN. The temporal course of this increase in extracellular NE concentration in the PVN coincided with the time course of inhibition elicited by the LC on the BRR response. Microinfusion of NE (10, 50, or 100 nM) into the parvocellular subnucleus of the PVN by reverse microdialysis also promoted a parallel increase in NE at the PVN and a reduction in the BRR response. Inhibition of the BRR response induced by microinjection into the PVN of the alpha 1-adrenoceptor agonist phenylephrine (10 nmol) or chemical activation of the LC was reversed by bilateral PVN microinjection of prazosin (100 pmol). However, local application to the PVN of the alpha 2- or beta-adrenoceptor agonist guanabenz (10 nmol) or isoproterenol (10 nmol) was ineffective. Our results suggest that NE released from the LC-PVN noradrenergic projection may participate in LC-induced suppression of the BRR response by activating the alpha 1-adrenoceptors at the parvocellular subnucleus of the PVN.

摘要

我们研究了在戊巴比妥麻醉下的成年Sprague-Dawley大鼠中,从蓝斑(LC)到下丘脑室旁核(PVN)的去甲肾上腺素能上行投射在LC诱导的压力感受器反射(BRR)反应抑制中的作用。基于体内微透析和高效液相色谱-电化学检测,向LC中微量注射L-谷氨酸(5 nmol)导致从PVN小细胞亚核收集的透析液中去甲肾上腺素(NE)浓度出现位点特异性增加。PVN中细胞外NE浓度的这种增加的时间进程与LC对BRR反应引发的抑制的时间进程一致。通过反向微透析向PVN的小细胞亚核微量注入NE(10、50或100 nM)也促进了PVN处NE的平行增加以及BRR反应的降低。双侧PVN微量注射哌唑嗪(100 pmol)可逆转向PVN微量注射α1-肾上腺素能激动剂去氧肾上腺素(10 nmol)或LC化学激活所诱导的BRR反应抑制。然而,向PVN局部应用α2-或β-肾上腺素能激动剂胍那苄(10 nmol)或异丙肾上腺素(10 nmol)无效。我们的结果表明,从LC-PVN去甲肾上腺素能投射释放的NE可能通过激活PVN小细胞亚核处的α1-肾上腺素能受体参与LC诱导的BRR反应抑制。

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