Exercise training attenuates hypertension and cardiac hypertrophy by modulating neurotransmitters and cytokines in hypothalamic paraventricular nucleus.
Exercise training attenuates hypertension and cardiac hypertrophy by modulating neurotransmitters and cytokines in hypothalamic paraventricular nucleus.
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运动训练通过调节下丘脑室旁核中的神经递质和细胞因子来减轻高血压和心脏肥大
DOI：
10.1371/journal.pone.0085481
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发表时间：
2014
期刊：
影响因子：
3.7
通讯作者：
Qin DN
中科院分区：
文献类型：
--
作者：
Jia LL;Kang YM;Wang FX;Li HB;Zhang Y;Yu XJ;Qi J;Suo YP;Tian ZJ;Zhu Z;Zhu GQ;Qin DN
目的规律运动作为一种有效的非药物降压疗法，有利于高血压的预防和控制，但其中枢机制尚不清楚。在这项研究中，我们假设慢性运动训练(EXT)通过上调抗炎细胞因子、减少促炎细胞因子(PIC)和恢复幼年自发性高血压大鼠(SHR)下丘脑室旁核(PVN)的神经递质平衡来延缓高血压的进展，减轻心肌肥厚。此外，我们还研究了核因子-κB(NF-κB)P65和NAD(P)H氧化酶在运动诱导效应中的作用。方法与结果正常血压的Wistar-京都(WKY)幼鼠和SHR大鼠分别给予中等强度的EXT 16周。SHR大鼠平均动脉压明显升高，心肌肥厚。自发性高血压大鼠的下丘脑室旁核谷氨酸、去甲肾上腺素(NE)、磷酸化IKKβ、核因子-κB P65活性、NAD(P)H氧化酶亚单位gp91Phox、PICs和单核细胞趋化因子蛋白-1水平升高，而γ-氨基丁酸和白介素10水平降低。这些SHR大鼠还表现出较高的肾交感神经活性(RSNA)、较高的血浆PIC水平和较低的IL-10水平。然而，Ext可改善SHR大鼠的上述变化。结论自发性高血压大鼠室旁核存在兴奋性和抑制性神经递质、促炎性和抗炎性细胞因子之间的失衡，至少部分参与了交感兴奋、高血压和心肌肥大；慢性运动训练通过恢复兴奋性和抑制性神经递质以及促炎性和抗炎性细胞因子之间的平衡来减轻高血压和心肌肥厚，核因子-κB和氧化应激可能参与了运动诱导的这些效应。
Aims Regular exercise as an effective non-pharmacological antihypertensive therapy is beneficial for prevention and control of hypertension, but the central mechanisms are unclear. In this study, we hypothesized that chronic exercise training (ExT) delays the progression of hypertension and attenuates cardiac hypertrophy by up-regulating anti-inflammatory cytokines, reducing pro-inflammatory cytokines (PICs) and restoring the neurotransmitters balance in the hypothalamic paraventricular nucleus (PVN) in young spontaneously hypertensive rats (SHR). In addition, we also investigated the involvement of nuclear factor-κB (NF-κB) p65 and NAD(P)H oxidase in exercise-induced effects. Methods and results Moderate-intensity ExT was administrated to young normotensive Wistar-Kyoto (WKY) and SHR rats for 16 weeks. SHR rats had a significant increase in mean arterial pressure and cardiac hypertrophy. SHR rats also had higher levels of glutamate, norepinephrine (NE), phosphorylated IKKβ, NF-κB p65 activity, NAD(P)H oxidase subunit gp91phox, PICs and the monocyte chemokine protein-1 (MCP-1), and lower levels of gamma-aminobutyric acid (GABA) and interleukin-10 (IL-10) in the PVN. These SHR rats also exhibited higher renal sympathetic nerve activity (RSNA), and higher plasma levels of PICs, and lower plasma IL-10. However, ExT ameliorates all these changes in SHR rats. Conclusion These findings suggest that there are the imbalances between excitatory and inhibitory neurotransmitters and between pro- and anti-inflammatory cytokines in the PVN of SHR rats, which at least partly contributing to sympathoexcitation, hypertension and cardiac hypertrophy; chronic exercise training attenuates hypertension and cardiac hypertrophy by restoring the balances between excitatory and inhibitory neurotransmitters and between pro- and anti-inflammatory cytokines in the PVN; NF-κB and oxidative stress in the PVN may be involved in these exercise-induced effects.
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