Hemodynamic effects of L-glutamate in NTS of conscious rats: a possible role of vascular nitrosyl factors

Hemodynamic effects of L-glutamate in NTS of conscious rats: a possible role of vascular nitrosyl factors
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DOI:
10.1152/ajpheart.1998.274.4.h1066
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发表时间:
1998-04-01
影响因子:
4.8
通讯作者:
Lewis, SJ
Lewis, SJ
中科院分区:
医学2区
文献类型:
--
作者:
Colombari, E;Davisson, RL;Lewis, SJ

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这项研究检查了将 L-谷氨酸 (L-Glu) 微量注射到清醒大鼠孤束核 (NTS) 中所产生的平均动脉血压、心率以及肾、肠系膜和后躯血管阻力变化的外周机制。 L-Glu 的显微注射在每个血管床中产生初始加压反应、心动过缓和血管收缩。随后观察到后躯血管舒张。给予哌唑嗪后,L-Glu 产生最初的低血压,这可能是由于心输出量减少所致。这种低血压之后是后躯血管舒张。一氧化氮合成的抑制并不影响哌唑嗪治疗大鼠的初始低血压或心动过缓,但在给予哌唑嗪和N-G-硝基-L-精氨酸甲酯(L-NAME)后首次微量注射L-Glu比单独给予哌唑嗪后产生显着更大的后肢血管舒张。第二次和第三次 L-Glu 显微注射产生明显较小的后躯血管舒张。我们得出的结论是:1)将 L-Glu 微注射到清醒大鼠的 NTS 中产生的血流动力学效应涉及交感神经系统的激活,2)预先形成的亚硝酰因子的释放可能介导后肢血管床的血管舒张。
This study examined peripheral mechanisms responsible for changes in mean arterial blood pressure, heart rate, and renal, mesenteric, and hindquarter vascular resistances produced by microinjections of L-glutamate (L-Glu) into the nucleus tractus solitarii (NTS) of conscious rats. Microinjection of L-Glu produced an initial presser response, bradycardia, and vasoconstriction in each vascular bed. Subsequent hindquarter vasodilation was observed. After prazosin was administered, L-Glu produced initial hypotension that was probably due to reduced cardiac output. This hypotension was followed by hindquarter vasodilation. Inhibition of nitric oxide synthesis did not affect the initial hypotension or bradycardia in rats treated with prazosin, but the first microinjection of L-Glu after administration of prazosin and N-G-nitro-L-arginine methyl ester (L-NAME) produced significantly greater hindquarter vasodilation than after administration of prazosin alone. Second and third microinjections of L-Glu produced significantly smaller hindquarter vasodilation. We conclude that 1) hemodynamic effects produced by microinjection of L-Glu into the NTS of conscious rats involves activation of the sympathetic nervous system and 2) release of preformed nitrosyl factors may mediate vasodilation in the hindquarter vascular bed.