Department of Nutrition & Exercise Physiology, University of Missouri, Columbia, Missouri, United States.
Department of Anesthesiology and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota, United States.
J Neurophysiol. 2024 Sep 1;132(3):1087-1097. doi: 10.1152/jn.00277.2024. Epub 2024 Aug 14.
Efferent muscle sympathetic nerve activity (MSNA) is under tonic baroreflex control. The arterial baroreflex exerts the strongest influence over medium-sized sympathetic action potential (AP) subpopulations in efferent MSNA recordings. Prior work from multiunit MSNA recordings has shown baroreflex loading selectively abolishes the sympathetic response to hypoxia. The purpose of the study was to examine baroreflex control over different-sized AP clusters and characterize the neural recruitment strategies of sympathetic AP subpopulations with baroreflex and combined baroreflex/chemoreflex (i.e., hypoxia) activation. We loaded the arterial baroreceptors [intravenous phenylephrine (PE)] alone and in combination with systemic hypoxia ([Formula: see text] 80%) in nine healthy young men. We extracted sympathetic APs using the wavelet-based methodology and quantified baroreflex gain for individual AP clusters. AP baroreflex threshold gain was measured as the slope of the linear relationship between AP probability versus diastolic blood pressure for 10 normalized clusters. Baroreflex loading with phenylephrine decreased MSNA and AP firing compared with baseline (all < 0.05). However, the phenylephrine-mediated decrease in AP firing was lost with concurrent hypoxia ( = 0.384). Compared with baseline, baroreflex loading reduced medium-sized AP cluster baroreflex threshold slope (condition = 0.005) and discharge probability (condition < 0.0001); these reductions from baseline were maintained during simultaneous hypoxia (both < 0.05). Present findings indicate a key modulatory role of the baroreceptors on medium-sized APs in blood pressure regulation that withstands competing signals from peripheral chemoreflex activation. This study provides a novel understanding on baroreflex control of efferent sympathetic nervous system activity during competing stressors: baroreflex loading and peripheral chemoreflex activation. We show chemoreflex activation buffers baroreflex-mediated reductions in sympathetic nervous system activity. More importantly, baroreflex loading reduced baroreflex threshold gain of sympathetic action potential clusters and this reduction withstood chemoreflex activation. These data suggest the arterial baroreflex holds a primary regulatory role over medium-sized sympathetic neurons despite competing chemoreflex signals.
传出肌交感神经活动（MSNA）受到紧张性压力反射控制。动脉压力反射对传出 MSNA 记录中的中型交感动作电位（AP）亚群施加最强的影响。来自多单位 MSNA 记录的先前工作表明，压力反射加载选择性地消除了缺氧对交感神经反应的影响。本研究的目的是检查不同大小 AP 簇的压力反射控制，并描述压力反射和联合压力反射/化学反射（即缺氧）激活对交感 AP 亚群的神经募集策略。我们单独加载动脉压力感受器（静脉注射苯肾上腺素（PE））并与全身缺氧（[Formula: see text] 80%）一起加载在 9 名健康年轻男性中。我们使用基于小波的方法提取交感 AP，并量化单个 AP 簇的压力反射增益。AP 压力反射阈值增益是通过 AP 概率与舒张压之间的线性关系的斜率来测量的，该斜率适用于 10 个归一化簇。与基线相比，用苯肾上腺素加载压力反射会降低 MSNA 和 AP 放电（均<0.05）。然而，苯肾上腺素介导的 AP 放电减少在同时缺氧时丢失（=0.384）。与基线相比，压力反射加载降低了中型 AP 簇压力反射阈值斜率（条件=0.005）和放电概率（条件<0.0001）；这些从基线开始的减少在同时缺氧时保持不变（均<0.05）。目前的研究结果表明，压力感受器对血压调节中型 AP 具有关键的调节作用，这种调节作用可以抵抗外周化学反射激活的竞争信号。本研究提供了对传出交感神经系统活动在竞争应激源（压力反射加载和外周化学反射激活）期间的压力反射控制的新认识。我们表明，化学反射激活缓冲了压力反射介导的交感神经系统活动的减少。更重要的是，压力反射加载降低了交感动作电位簇的压力反射阈值增益，并且这种降低可以承受化学反射的激活。这些数据表明，尽管存在竞争的化学反射信号，动脉压力反射仍然对中型交感神经元具有主要的调节作用。
