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Sympathetic and angiotensinergic responses mediated by paradoxical sleep loss in rats

机译:大鼠反常睡眠丧失介导的交感和血管紧张素反应

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Introduction: Recent investigations over the past decade have linked the development of hypertension to sleep loss, although the mechanisms underlying this association are still under scrutiny. To determine the relationship between sleep deprivation and cardiovascular dysfunction, we examined the effects of paradoxical sleep deprivation on heart rate, blood pressure, sympathetic nerve activity (SNA) and their consequences in the blood renin-angiotensin system.Materials and methods: Wistar-Hannover male rats were randomly assigned to three experimental groups: 1) control, 2) paradoxical sleep deprivation for 24 h and 3) paradoxical sleep deprivation for 96 h. Blood pressure and heart rate were recorded in awake, freely moving rats.Results: Heart rate was higher in the 96 h paradoxical sleep deprivation group compared with the control group. Renal SNA was increased in all deprived groups. However, no significant statistical differences were observed in blood pressure or splanchnic SNA among groups. Paradoxical sleep deprivation (24 and 96 h) reduced plasma angiotensin II (Ang II) concentrations.Conclusions: the results suggest that selective sleep deprivation produces an increase in SNA, preferentially in the kidney. Thus, alterations in the sympathetic system in response to sleep loss may be an important pathway through which hypertension develops.
机译:简介:过去十年来的最新研究已将高血压的发生与睡眠丧失联系在一起,尽管这种关联的潜在机制仍在审查中。为了确定睡眠剥夺与心血管功能障碍之间的关系,我们研究了自相矛盾的睡眠剥夺对心率,血压,交感神经活动(SNA)的影响及其对血液肾素-血管紧张素系统的影响。材料和方法:Wistar-Hannover将雄性大鼠随机分为三个实验组:1)对照组,2)自相矛盾的睡眠剥夺24小时和3)自相矛盾的睡眠剥夺96h。结果:96小时悖论性睡眠剥夺组的心率高于对照组。所有贫困人群的肾脏SNA均升高。但是,各组之间的血压或内脏SNA均未观察到显着的统计学差异。矛盾的睡眠剥夺(24和96 h)降低血浆血管紧张素II(Ang II)的浓度。结论:结果表明选择性睡眠剥夺会导致SNA升高,尤其是肾脏。因此,响应睡眠丧失的交感系统改变可能是高血压发展的重要途径。

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