Corticotropin releasing factor excites neurons of posterior hypothalamic nucleus to produce tachycardia in rats

Corticotropin releasing factor excites neurons of posterior hypothalamic nucleus to produce tachycardia in rats
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促肾上腺皮质激素释放因子兴奋下丘脑后核神经元产生大鼠心动过速

DOI:
10.1038/srep20206
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发表时间:
2016-02-01
期刊:
影响因子:
4.6
通讯作者:
Zhu, Jing-Ning
Zhu, Jing-Ning
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Gao, He-Ren;Zhuang, Qian-Xing;Zhu, Jing-Ning

文献摘要

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促肾上腺皮质激素释放因子(CRF)是一种参与应激反应的肽激素,在心血管调节中起着关键作用。在这里,我们报道了CRF对心血管活动的中心作用是由下丘脑后核(PH)介导的,这是一个负责应激诱导心血管变化的重要结构。我们目前的研究结果表明,CRF通过两个CRF受体CRFR1和CRFR2直接激活PH神经元,从而增加心率(HR),而不是平均动脉压(MAP)和肾交感神经活动(RSNA)。双侧迷走神经切断术对PH内微量注射CRF的心动过速反应没有影响,而β肾上腺素能受体拮抗剂心得安几乎完全消除了心动过速。此外,在PH中微注射CRF主要增加了延髓吻侧腹外侧(RVLM)和延髓吻侧腹内侧(RVMM)的神经元活动,但不影响迷走神经背侧运动核(DMNV)的神经元活动。这些发现表明,PH是中枢CRF系统调节心脏活动的关键靶点,PH- rvlm / rvmm -心脏交感神经通路,而不是PH- dmnv -迷走神经通路,可能参与CRF诱导的心动过速。
Corticotropin releasing factor (CRF), a peptide hormone involved in the stress response, holds a key position in cardiovascular regulation. Here, we report that the central effect of CRF on cardiovascular activities is mediated by the posterior hypothalamic nucleus (PH), an important structure responsible for stress-induced cardiovascular changes. Our present results demonstrate that CRF directly excites PH neurons via two CRF receptors, CRFR1 and CRFR2 and consequently increases heart rate (HR) rather than the mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA). Bilateral vagotomy does not influence the tachycardia response to microinjection of CRF into the PH, while β adrenergic receptor antagonist propranolol almost totally abolishes the tachycardia. Furthermore, microinjecting CRF into the PH primarily increases neuronal activity of the rostral ventrolateral medulla (RVLM) and rostral ventromedial medulla (RVMM), but does not influence that of the dorsal motor nucleus of the vagus nerve (DMNV). These findings suggest that the PH is a critical target for central CRF system in regulation of cardiac activity and the PH-RVLM/RVMM-cardiac sympathetic nerve pathways, rather than PH-DMNV-vagus pathway, may contribute to the CRF-induced tachycardia.