The pedunculopontine tegmentum controls renal sympathetic nerve activity and cardiorespiratory activities in nembutal-anesthetized rats.

The pedunculopontine tegmentum controls renal sympathetic nerve activity and cardiorespiratory activities in nembutal-anesthetized rats.
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DOI:
10.1371/journal.pone.0187956
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发表时间:
2017
期刊:
影响因子:
3.7
通讯作者:
Carley DW
Carley DW
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Fink AM;Dean C;Piano MR;Carley DW

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肾交感神经活动(RSNA)升高伴随着各种复杂的疾病,包括阻塞性睡眠呼吸暂停,心力衰竭和慢性肾脏疾病。了解肾脏的病理生理机制对于确定为什么高血压是这些疾病的常见后遗症和诱发因素是很重要的。脑干在调节RSNA中的作用仍不完全清楚。脚桥被盖(PPT)是已知的调节行为,包括警觉性,运动和快速眼动睡眠。在麻醉大鼠中,PPT神经元的激活先前被发现增加内脏交感神经活动和血压,除了改变呼吸。本研究是PPT及其在调节RSNA中的潜在作用的第一次调查。在Nembutal麻醉的大鼠中,使用DL-同型半胱氨酸(DLH)的显微注射以100 μm的增量探测PPT,以确定有效部位,定义为可以诱发RSNA变化的位置。在18只大鼠中共进行了239次DLH显微注射,确定了20个有效部位(每个部位都能引起可重复的交感神经兴奋反应)。RSNA峰值增加发生在PPT激活后10-20秒内,RSNA较基线增加104.5 ± 68.4%(平均值±标准差)。平均动脉压持续显著升高30秒,从101.6 ± 18.6 mmHg升高至135.9 ± 36.4 mmHg。DLH微量注射也增加呼吸频率和每分钟通气量。有效部位分布于PPT的喙尾侧,主要位于核的背侧。用DLH显微注射测试的大多数PPT位置没有改变RSNA(179个位点),这表明赋予肾交感神经兴奋功能的神经元包括PPT的一小部分。该研究还强调了进一步研究的重要性,以确定交感兴奋性PPT神经元是否有助于阻塞性睡眠呼吸暂停和心力衰竭等疾病的不良肾脏和心血管后果。
Elevated renal sympathetic nerve activity (RSNA) accompanies a variety of complex disorders, including obstructive sleep apnea, heart failure, and chronic kidney disease. Understanding pathophysiologic renal mechanisms is important for determining why hypertension is both a common sequelae and a predisposing factor of these disorders. The role of the brainstem in regulating RSNA remains incompletely understood. The pedunculopontine tegmentum (PPT) is known for regulating behaviors including alertness, locomotion, and rapid eye movement sleep. Activation of PPT neurons in anesthetized rats was previously found to increase splanchnic sympathetic nerve activity and blood pressure, in addition to altering breathing. The present study is the first investigation of the PPT and its potential role in regulating RSNA. Microinjections of DL-homocysteic acid (DLH) were used to probe the PPT in 100-μm increments in Nembutal-anesthetized rats to identify effective sites, defined as locations where changes in RSNA could be evoked. A total of 239 DLH microinjections were made in 18 rats, which identified 20 effective sites (each confirmed by the ability to evoke a repeatable sympathoexcitatory response). Peak increases in RSNA occurred within 10–20 seconds of PPT activation, with RSNA increasing by 104.5 ± 68.4% (mean ± standard deviation) from baseline. Mean arterial pressure remained significantly elevated for 30 seconds, increasing from 101.6 ± 18.6 mmHg to 135.9 ± 36.4 mmHg. DLH microinjections also increased respiratory rate and minute ventilation. The effective sites were found throughout the rostal-caudal extent of the PPT with most located in the dorsal regions of the nucleus. The majority of PPT locations tested with DLH microinjections did not alter RSNA (179 sites), suggesting that the neurons that confer renal sympathoexcitatory functions comprise a small component of the PPT. The study also underscores the importance of further investigation to determine whether sympathoexcitatory PPT neurons contribute to adverse renal and cardiovascular consequences of diseases such as obstructive sleep apnea and heart failure.
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