Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans.

Arterial baroreflex control of muscle sympathetic nerve activity under orthostatic stress in humans.
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DOI:
10.3389/fphys.2012.00314
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发表时间:
2012
影响因子:
4
通讯作者:
Nishiyasu T
Nishiyasu T
中科院分区:
医学2区
文献类型:
--
作者:
Ichinose M;Nishiyasu T

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维持血压以抵抗重力对体内液体分布的影响所引起的直立应力的机制是生理学中的重要问题,特别是对于通常采取直立姿势的人类而言。外周血管收缩和心率增加 (HR) 是心血管对体位性应激的主要调节,并构成通过颈动脉窦和主动脉压力感受器(动脉压力感受器:ABR)和心肺牵张感受器(心肺压力感受器)引起的反射反应的一部分。在一系列研究中,我们一直在对人体施加直立应激时,描述了 ABR 介导的心血管血流动力学和肌肉交感神经活动 (MSNA) 的调节。我们发现,在直立性应激下,动态颈动脉压力反射反应受到调节,颈动脉压力反射卸载引起的 MSNA、血压和 HR 反应增加,MSNA 抑制时间更短,平均动脉血压 (MAP) 相应降低和更快恢复,对颈动脉压力反射刺激的 HR 反应更大。我们的结果还表明,随着直立性应激的增加,ABR 介导的对爆发发生率、爆发强度和总 MSNA 的逐搏控制逐渐调节,直至诱发晕厥,并且在晕厥发生期间,ABR 对上述 MSNA 变量的控制敏感性大大降低。我们认为,在人类中,直立性应激下 ABR 功能的调节可能是维持血压和限制直立性低血压的机制之一,而 ABR 对交感血管舒缩活动的控制受损会导致与直立性晕厥相关的严重低血压。
The mechanisms by which blood pressure is maintained against the orthostatic stress caused by gravity's effect on the fluid distribution within the body are important issues in physiology, especially in humans who usually adopt an upright posture. Peripheral vasoconstriction and increased heart rate (HR) are major cardiovascular adjustments to orthostatic stress and comprise part of the reflex response elicited via the carotid sinus and aortic baroreceptors (arterial baroreflex: ABR) and cardiopulmonary stretch receptors (cardiopulmonary baroreflex). In a series of studies, we have been characterizing the ABR-mediated regulation of cardiovascular hemodynamics and muscle sympathetic nerve activity (MSNA) while applying orthostatic stress in humans. We have found that under orthostatic stress, dynamic carotid baroreflex responses are modulated as exemplified by the increases in the MSNA, blood pressure, and HR responses elicited by carotid baroreflex unloading and the shorter period of MSNA suppression, comparable reduction and faster recovery of mean arterial blood pressure (MAP) and greater HR response to carotid baroreflex stimulation. Our results also show that ABR-mediated beat-to-beat control over burst incidence, burst strength and total MSNA is progressively modulated as orthostatic stress is increased until induction of syncope, and that the sensitivity of ABR control over the aforementioned MSNA variables is substantially reduced during the development of syncope. We suggest that in humans, the modulation of ABR function under orthostatic stress may be one of the mechanisms by which blood pressure is maintained and orthostatic hypotension limited, and impairment of ABR control over sympathetic vasomotor activity leads to the severe hypotension associated with orthostatic syncope.
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发表时间: 2004-10-01
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发表时间: 1972-01-01
期刊: ACTA PHYSIOLOGICA SCANDINAVICA
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发表时间: 2002-11-01
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