Regulation of arterial pressure by the paraventricular nucleus in conscious rats: interactions among glutamate, GABA, and nitric oxide.

Regulation of arterial pressure by the paraventricular nucleus in conscious rats: interactions among glutamate, GABA, and nitric oxide.
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DOI:
10.3389/fphys.2012.00490
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发表时间:
2012
影响因子:
4
通讯作者:
Hasser EM
Hasser EM
中科院分区:
医学2区
文献类型:
--
作者:
Martins-Pinge MC;Mueller PJ;Foley CM;Heesch CM;Hasser EM

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下丘脑室旁核(PVN)是植物神经和神经内分泌调节的重要部位。在麻醉动物和体外实验表明γ-氨基丁酸(GABA),一氧化氮(NO),和谷氨酸在PVN之间的相互作用。PVN的心血管作用和这些神经递质在清醒动物中的相互作用尚未得到充分评价。在慢性仪器清醒大鼠,平均动脉压(MAP)和心率(HR)的反应,微量注射(100 nl)在该地区的PVN进行了测试。双侧阻断PVN中的离子型兴奋性氨基酸(EAA)受体(犬尿烯酸,Kyn)可使MAP和HR显著降低。GABAA受体阻断(荷包牡丹碱,Bic)和抑制NO合酶[(NOS),N-(G)-单甲基-L-精氨酸,L-NMMA]均使MAP和HR升高。NO供体硝普钠(SNP)可产生降压反应,但Bic可减弱该反应。NOS抑制增强升压反应的选择性EAA激动剂,N-甲基-D-天冬氨酸(NMDA),和降压反应的Kyn。事先阻断EAA受体可减弱Bic引起的MAP和HR增加。因此,对GABA阻断的升压反应需要EAA受体,并且GABA神经传递有助于NO抑制。紧张性兴奋效应谷氨酸在PVN的紧张性衰减NO。这些数据表明,在PVN的清醒大鼠,GABA,谷氨酸,和NO相互作用在一个复杂的方式来调节动脉压和HR在正常条件下。
The paraventricular nucleus (PVN) of the hypothalamus is an important site for autonomic and neuroendocrine regulation. Experiments in anesthetized animals and in vitro indicate an interaction among gamma-aminobutyric acid (GABA), nitric oxide (NO), and glutamate in the PVN. The cardiovascular role of the PVN and interactions of these neurotransmitters in conscious animals have not been evaluated fully. In chronically instrumented conscious rats, mean arterial pressure (MAP) and heart rate (HR) responses to microinjections (100 nl) in the region of the PVN were tested. Bilateral blockade of ionotropic excitatory amino acid (EAA) receptors (kynurenic acid, Kyn) in the PVN produced small but significant decreases in MAP and HR. GABAA receptor blockade (bicuculline, Bic), and inhibition of NO synthase [(NOS), N-(G)-monomethyl-L-arginine, L-NMMA] each increased MAP and HR. The NO donor sodium nitroprusside (SNP) produced depressor responses that were attenuated by Bic. NOS inhibition potentiated both pressor responses to the selective EAA agonist, N-methyl-D-aspartic acid (NMDA), and depressor responses to Kyn. Increases in MAP and HR due to Bic were blunted by prior blockade of EAA receptors. Thus, pressor responses to GABA blockade require EAA receptors and GABA neurotransmission contributes to NO inhibition. Tonic excitatory effects of glutamate in the PVN are tonically attenuated by NO. These data demonstrate that, in the PVN of conscious rats, GABA, glutamate, and NO interact in a complex fashion to regulate arterial pressure and HR under normal conditions.
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