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通过向清醒大鼠的孤束核微量注射NMDA受体拮抗剂,压力感受性反射性心动过缓的增益降低。

The gain of the baroreflex bradycardia is reduced by microinjection of NMDA receptor antagonists into the nucleus tractus solitarii of awake rats.

作者信息

Frigero M, Bonagamba L G, Machado B H

机构信息

Department of Physiology, School of Medicine of Ribeirão Preto, USP, 14049-900, Ribeirão Preto, Brazil.

出版信息

J Auton Nerv Syst. 2000 Feb 14;79(1):28-33. doi: 10.1016/s0165-1838(99)00089-2.

Abstract

The baroreflex activation with phenylephrine infusion produces a bradycardic response. In the present study, the role of NMDA receptors in the nucleus tractus solitarii (NTS) in the processing of the parasympathetic component of the baroreflex was evaluated using acid phosphonivaleric (AP-5), a selective NMDA receptor antagonist. Baroreflex activation was performed before and after bilateral microinjection of AP-5 into the intermediate commissural NTS (0.5 mm lateral to the midline). Microinjection of the vehicle (saline, 0.9%) or a dose of 2 nmol/50 nl of AP-5 into the NTS produced no effect on the gain of the baroreflex while a dose of 10 nmol/50 nl of AP-5 produced a significant reduction in the gain of the baroreflex 2 min after microinjection [-1.43+/-0.22 vs. -0. 43+/-0.03 bpm/mmHg, (n=6)], with a return to control levels 10 min after the microinjections. The dose of 10 nmol/50 nl was selective for NMDA receptors considering that the cardiovascular responses to microinjection of AMPA (0.05 pmol/50 nl), a non-NMDA receptor agonist, were not affected by this dose of AP-5 and the responses to microinjection of NMDA (2 nmol/50 nl) were blocked. The data show that the bradycardic response to baroreflex activation was blocked by AP-5 microinjected into the NTS, indicating that the neurotransmission of the parasympathetic component of the baroreflex is mediated by NMDA receptors in the NTS.

摘要

苯肾上腺素输注激活压力反射会产生心动过缓反应。在本研究中,使用选择性N-甲基-D-天冬氨酸(NMDA)受体拮抗剂酸膦戊酸(AP-5)评估孤束核(NTS)中NMDA受体在压力反射副交感神经成分处理过程中的作用。在双侧向中间联合NTS(中线外侧0.5 mm)微量注射AP-5之前和之后进行压力反射激活。向NTS微量注射溶媒(生理盐水,0.9%)或2 nmol/50 nl剂量的AP-5对压力反射增益无影响,而10 nmol/50 nl剂量的AP-5在微量注射后2分钟使压力反射增益显著降低[-1.43±0.22 vs. -0.43±0.03 bpm/mmHg,(n = 6)],微量注射后10分钟恢复到对照水平。考虑到对非NMDA受体激动剂AMPA(0.05 pmol/50 nl)微量注射的心血管反应不受该剂量AP-5影响,且对NMDA(2 nmol/50 nl)微量注射的反应被阻断,10 nmol/50 nl剂量对NMDA受体具有选择性。数据表明,向NTS微量注射AP-5可阻断对压力反射激活的心动过缓反应,这表明压力反射副交感神经成分的神经传递由NTS中的NMDA受体介导。

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