RESULTS: Twenty-one days of CIH induced autonomic imbalance and hypertension in rats. Notably, acute chemogenetic inhibition (CNO) of medullary NTS astrocytes using Designer Receptors Exclusively Activated by Designers Drugs (DREADD) restored normal cardiac variability (LF/HF: 1.1 ± 0.2 vs. 2.4 ± 0.2 vs. 1.4 ± 0.3, Sham vs. CIH vs. CIH + CNO, respectively) and markedly reduced arterial blood pressure in rats exposed to CIH (MABP: 82.7 ± 1.2 vs. 104.8 ± 4.4 vs. 89.6 ± 0.9 mmHg, Sham vs. CIH vs. CIH + CNO, respectively). In addition, the potentiated sympathoexcitation elicit by acute hypoxic chemoreflex activation in rats exposed to CIH was also completely abolished by chemogenetic inhibition of NTS astrocytes using DREADDs.
CONCLUSIONS: Our results support a role for NTS astrocytes in the maintenance of heightened sympathetic drive and hypertension during chronic exposure to intermittent hypoxia mimicking OSA.
结果:21天的CIH诱发大鼠自主神经失衡和高血压。值得注意的是,使用设计师专用受体(DREADD)恢复的正常心脏变异性(LF/HF:1.1±0.2vs.2.4±0.2vs.1.4±0.3,Shamvs.CIHvs.CIH+CNO,分别)和显着降低暴露于CIH的大鼠的动脉血压(MABP:82.7±1.2vs.104.8±4.4vs.89.6±0.9mmHg,Shamvs.CIHvs.CIH+CNO,分别)。此外,通过使用DREADDs对NTS星形胶质细胞的化学遗传学抑制,也完全消除了暴露于CIH的大鼠急性低氧化学反射激活引起的交感神经兴奋.
结论:我们的结果支持NTS星形胶质细胞在长期暴露于模拟OSA的间歇性缺氧期间维持增强的交感神经驱动和高血压中的作用。