Presympathetic neuron dysfunction--time to reconsider increased intrinsic activity as the cause of neurogenic hypertension.
Presympathetic neuron dysfunction--time to reconsider increased intrinsic activity as the cause of neurogenic hypertension.
复制标题
前交感神经元功能障碍——是时候重新考虑内在活动增加是神经源性高血压的原因了。
DOI：
10.1113/expphysiol.2014.080077
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发表时间：
2014
影响因子：
2.7
通讯作者：
Wainford,RD
中科院分区：
文献类型：
--
作者：
Wainford,RD
In this issue, there is a paradigm-shifting article (Almado et al., 2014) that examines the effect of chronic intermittent hypoxia (CIH)(which stimulates the development of neurogenic hypertension) on the intrinsic electrophysiological properties of rostral ventrolateral medulla (RVLM) pre-sympathetic neurons in juvenile rats. The authors provide the first experimental evidence that both pre-sympathetic and phrenic nucleus-projecting neurons of the RVLM exhibit the characteristics of intrinsic pacemakers in juvenile rats. Significantly, the authors present experimental data demonstrating that the stress of chronic intermittent hypoxia (CIH), which evokes neurogenic hypertension, produces no change in the electrophysical properties of these RVLM neurons. These findings challenge the prevailing hypothesis that increased activity of pre-sympathetic neurons is the source of enhanced sympathetic drive during neurogenic hypertension. This study is the first report of the impact of CIH on the neural activity of RVLM neurons in juvenile animals, in which there is full expression of functional ion channels and synaptic receptors compared to neonatal rats in which prior studies have been conducted. As such, these findings, generated in animals of a significantly older age than was previously reported, are likely more representative of the impact of CIH on RVLM neural activity in the fully developed adult brain than studies conducted in neonatal animals. Owing to the significant global adverse health impact of hypertension, studies such as these, which suggest new directions in which to direct studies designed to elucidate the mechanisms driving neurogenic hypertension have potential high significance for human health.It has been long held that pre-sympathetic neurons in the RVLM are the source of sympathetic activity and it has been postulated that changes in the intrinsic properties (ie, increased activity) of these neurons are the main causal mechanism for the development of sympathetic overactivation and neurogenic hypertension. There are considerable challenges in measuring the activity of these pre-sympathetic neurons–as such this hypothesis is predominantly supported by data generated in neonatal rats exhibiting a still developing central nervous system. Recently work by several pioneering groups (Degacheva et al., 2013; Gao & Derbenev, 2013) has facilitated the study of this neuronal population in brainstem slices from juvenile rats–a significant technical achievement. The studies presented by Almado et al., in this issue of Experimental Physiology utilize the same technical advancements to
