Exaggerated sympathetic and cardiovascular responses to stimulation of the mesencephalic locomotor region in spontaneously hypertensive rats.
Exaggerated sympathetic and cardiovascular responses to stimulation of the mesencephalic locomotor region in spontaneously hypertensive rats.
复制标题
DOI：
10.1152/ajpheart.00479.2015
复制
发表时间：
2016
期刊：
影响因子：
--
通讯作者：
N. Liang;Jere H. Mitchell;Scott A. Smith;M. Mizuno
中科院分区：
文献类型：
--
作者：
N. Liang;Jere H. Mitchell;Scott A. Smith;M. Mizuno
高血压患者对运动的交感神经和压力反应被夸大了。然而，导致这种异常的潜在机制仍未完全阐明。中央指令是一种源自大脑高级中枢的神经驱动，已知可以同时激活心血管和运动控制回路。因此，它是在这种疾病中产生增强血管反应的可行候选者。我们假设中枢指挥功能的增强有助于高血压患者心血管对运动的反应增强。为了验证这一假设，我们在失脑、瘫痪的正常血压Wistar-Kyoto （WKY）和自发性高血压大鼠（SHR）中，检测了中脑运动区（MLR; 20-50 μA， 10 μA步诱发有效运动）电刺激时肾交感神经活动（RSNA）和平均动脉压（MAP）的变化。MLR刺激时胫骨神经放电在WKY和SHR组均呈强度依赖性显著增加，但组间无差异。刺激MLR后，两组RSNA和MAP均随刺激强度的增加而显著增加。重要的是，在所有刺激强度下（例如，在50 μA时，ΔRSNA: WKY 153±31%,SHR 287±42%；ΔMAP: WKY 87±9 mmHg, SHR 139±7 mmHg）， SHR对这种有效运动的交感神经和压力反应的增加明显大于WKY。这些发现提供了第一个证据，证明中央指挥可能是高血压患者运动时交感神经活动和血压过度升高的关键因素。
The sympathetic and pressor responses to exercise are exaggerated in hypertension. However, the underlying mechanisms causing this abnormality remain to be fully elucidated. Central command, a neural drive originating in higher brain centers, is known to activate cardiovascular and locomotor control circuits concomitantly. As such, it is a viable candidate for the generation of the augmented vascular response to exercise in this disease. We hypothesized that augmentations in central command function contribute to the heightened cardiovascular response to exercise in hypertension. To test this hypothesis, changes in renal sympathetic nerve activity (RSNA) and mean arterial pressure (MAP) in response to electrical stimulation of mesencephalic locomotor region (MLR; 20-50 μA in 10-μA steps evoking fictive locomotion), a putative component of the central command pathway, were examined in decerebrate, paralyzed normotensive Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHR). Tibial nerve discharge during MLR stimulation significantly increased in an intensity-dependent manner in both WKY and SHR but was not different between groups. Stimulation of the MLR evoked significantly larger increases in RSNA and MAP with increasing stimulation intensity in both groups. Importantly, the increases in sympathetic and pressor responses to this fictive locomotion were significantly greater in SHR compared with WKY across all stimulation intensities (e.g., at 50 μA, ΔRSNA: WKY 153 ± 31%, SHR 287 ± 42%; ΔMAP: WKY 87 ± 9 mmHg, SHR 139 ± 7 mmHg). These findings provide the first evidence that central command may be a critical contributor to the exaggerated rise in sympathetic activity and blood pressure during exercise in hypertension.