Hosseiniravesh Mohammad Reza, Hojati Vida, Khajavirad Abolfazl, Shajiee Hooman, Shafei Mohammad Naser, Mohebbati Reza
Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran.
Department of Physiology, Faculty of Medicine, Mashhad University of Medical Sciences, Mashhad, Iran.
Iran J Basic Med Sci. 2022 May;25(5):569-576. doi: 10.22038/IJBMS.2022.62431.13809.
In the present study, the cardiovascular effects of glutamate NMDA receptor of the pedunculopontine tegmental nucleus (PPT) in normotensive and hydralazine (HLZ) hypotensive rats were evaluated.
In the normotensive condition, MK-801(1 nmol; an NMDA receptor antagonist) and L-glutamate (L-Glu, 50 nmol an agonist) alone and together were microinjected into the nucleus using a stereotaxic device. In hypotensive condition, 2 min after induction of hypotension by HLZ (10 mg/kg, intravenous), drugs, same as in normotensive condition, were microinjected into the PPT. Recorded mean arterial pressure (MAP), systolic blood pressure (SBP), and heart rate (HR) were recorded throughout the experiment by a Power lab apparatus that was connected to a catheter inserted into the femoral arty. The cardiovascular changes (Δ) induced by microinjection drugs were computed and statistically analyzed.
In the normotensive condition, L-Glu significantly increased ΔMAP and ΔSBP (<0.001) and decreased ΔHR (<0.01) compared with the control. MK-801 alone significantly increased HR (<0.05) while co-injected with L-Glu + MK-801 it significantly attenuated the L-Glu effect on ΔMAP and ΔSBP but augmented ΔHR (<0.01). In the hydralazine hypotension condition, L-Glu significantly improved hypotension (<0.01) and deteriorated bradycardia induced by HLZ (<0.05). MK-801 alone did not significantly affect ΔMAP, ΔSBP, and ΔHR but when co-injected with L-Glu (L-Glu + MK-801) it could significantly attenuate the cardiovascular effect of L-Glu in the PPT.
We found that activation of NMDA receptors of the glutamatergic system in the PPT evoked blood pressure and inhibited HR in both normotensive and hypotensive conditions in rats.
在本研究中，评估了在正常血压和肼屈嗪（HLZ）诱导的低血压大鼠中，脚桥被盖核（PPT）的谷氨酸N-甲基-D-天冬氨酸（NMDA）受体对心血管系统的影响。
在正常血压状态下，使用立体定位装置将单独的MK-801（1纳摩尔；一种NMDA受体拮抗剂）和L-谷氨酸（L-Glu，50纳摩尔，一种激动剂）以及二者联合微量注射到该核团中。在低血压状态下，静脉注射HLZ（10毫克/千克）诱导低血压2分钟后，将与正常血压状态下相同的药物微量注射到PPT中。在整个实验过程中，通过连接到插入股动脉的导管的Powerlab仪器记录平均动脉压（MAP）、收缩压（SBP）和心率（HR）。计算并统计分析微量注射药物引起的心血管变化（Δ）。
在正常血压状态下，与对照组相比，L-Glu显著增加了ΔMAP和ΔSBP（<0.001），并降低了ΔHR（<0.01）。单独使用MK-801显著增加了HR（<0.05），而与L-Glu + MK-801联合注射时，它显著减弱了L-Glu对ΔMAP和ΔSBP的作用，但增加了ΔHR（<0.01）。在肼屈嗪诱导的低血压状态下，L-Glu显著改善了低血压（<0.01），并加剧了HLZ诱导的心动过缓（<0.05）。单独使用MK-801对ΔMAP、ΔSBP和ΔHR没有显著影响，但与L-Glu联合注射（L-Glu + MK-801）时，它可以显著减弱L-Glu在PPT中的心血管效应。
我们发现，在正常血压和低血压状态下，激活PPT中谷氨酸能系统的NMDA受体会诱发大鼠血压升高并抑制心率。
