PDF(Pubmed)
Abstract：
BACKGROUND: Hypertension, a leading cause of death, was investigated in this study to understand the role of specific brain regions in regulating blood pressure. The lateral parabrachial nucleus (LPBN), Kolliker-fuse nucleus (KF), and periductal grey matter (PAG) were examined for their involvement in hypertension.
METHODS: Lentiviral vectors were used to alter the activity of these brain regions in hypertensive rats. Over a 75-day period, blood pressure, heart rate, reflex responses, and heart rate variability were measured.
RESULTS: Decreasing the activity in the LPBN resulted in a reduced sympathetic outflow, lowering the blood pressure and heart rate. In the KF, the sympathetic activity decreased and chemoreflex variation was attenuated, without affecting the blood pressure. Silencing the PAG had no significant impact on blood pressure or sympathetic tone, but decreased cardiac baroreflex gain.
CONCLUSIONS: These findings highlight the significant role of the LPBN in hypertension-related sympathetic activation. Additionally, LPBN and KF neurons appear to activate mechanisms that control respiration and sympathetic outflow during chemoreceptor activation.
CONCLUSIONS: The study provided insights into the contribution of the midbrain and pontine regions to neurogenic hypertension and offers potential avenues for future genetic interventions and developing novel treatment approaches.
METHODS: Lentiviral vectors were used to alter the activity of these brain regions in hypertensive rats. Over a 75-day period, blood pressure, heart rate, reflex responses, and heart rate variability were measured.
RESULTS: Decreasing the activity in the LPBN resulted in a reduced sympathetic outflow, lowering the blood pressure and heart rate. In the KF, the sympathetic activity decreased and chemoreflex variation was attenuated, without affecting the blood pressure. Silencing the PAG had no significant impact on blood pressure or sympathetic tone, but decreased cardiac baroreflex gain.
CONCLUSIONS: These findings highlight the significant role of the LPBN in hypertension-related sympathetic activation. Additionally, LPBN and KF neurons appear to activate mechanisms that control respiration and sympathetic outflow during chemoreceptor activation.
CONCLUSIONS: The study provided insights into the contribution of the midbrain and pontine regions to neurogenic hypertension and offers potential avenues for future genetic interventions and developing novel treatment approaches.
摘要：
背景：高血压，导致死亡的主要原因,在这项研究中进行了调查，以了解特定大脑区域在调节血压中的作用。外侧臂旁核(LPBN),Kolliker融合核(KF),检查导管周围灰质（PAG）是否参与高血压。
方法:使用慢病毒载体改变高血压大鼠这些脑区的活性。在75天的时间里，血压,心率,反射反应,测量心率变异性。
结果：减少LPBN的活动导致交感神经流出减少，降低血压和心率。在KF中,交感神经活动减少，化学反射变异减弱，而不影响血压。沉默PAG对血压或交感神经张力没有显著影响，但心脏压力反射增益降低。
结论：这些发现强调了LPBN在高血压相关交感神经激活中的重要作用。此外,LPBN和KF神经元似乎在化学感受器激活期间激活控制呼吸和交感神经流出的机制。
结论：该研究提供了对中脑和脑桥区域对神经源性高血压的贡献的见解，并为未来的遗传干预和开发新的治疗方法提供了潜在的途径。
方法:使用慢病毒载体改变高血压大鼠这些脑区的活性。在75天的时间里，血压,心率,反射反应,测量心率变异性。
结果：减少LPBN的活动导致交感神经流出减少，降低血压和心率。在KF中,交感神经活动减少，化学反射变异减弱，而不影响血压。沉默PAG对血压或交感神经张力没有显著影响，但心脏压力反射增益降低。
结论：这些发现强调了LPBN在高血压相关交感神经激活中的重要作用。此外,LPBN和KF神经元似乎在化学感受器激活期间激活控制呼吸和交感神经流出的机制。
结论：该研究提供了对中脑和脑桥区域对神经源性高血压的贡献的见解，并为未来的遗传干预和开发新的治疗方法提供了潜在的途径。
