Baltatu O, Janssen B J, Bricca G, Plehm R, Monti J, Ganten D, Bader M
Max-Delbrück-Center for Molecular Medicine, Berlin-Buch, Germany.
Hypertension. 2001 Feb;37(2 Pt 2):408-13. doi: 10.1161/01.hyp.37.2.408.
To study whether the brain renin-angiotensin system plays a role in the long-term and short-term control of blood pressure and heart rate variability, we examined in transgenic rats [TGR(ASrAOGEN)] with low brain angiotensinogen levels the 24-hour variation of blood pressure and heart rate. Telemetry recordings were made during basal and hypertensive conditions induced by a low-dose subcutaneous infusion of angiotensin II for 7 days. Short-term blood pressure and heart rate variability were evaluated by spectral analysis, and as a measure of baroreflex sensitivity, the average transfer gain between the pressure and heart rate variations was calculated. During the angiotensin II infusion in control but not TGR(ASrAOGEN) rats, the 24-hour rhythm of blood pressure was inverted (5.8+/-2 versus -0.4+/-1.8 mm Hg/group of day-night differences of blood pressure, P<0.05, respectively). In both the control and TGR(ASrAOGEN) rats, the 24-hour heart rate rhythms remained unaltered and paralleled those of locomotor activity. The transfer gain between 0.3 to 0.6 Hz was significantly higher in TGR(ASrAOGEN) than in control rats during control (0.71+/-0.1 versus 0.35+/-0.06, P<0.05) but not during angiotensin II infusion (0.6+/-0.07 versus 0.4+/-0.1, P>0.05). These results demonstrate that the brain renin-angiotensin system plays an important role in mediating the effects of angiotensin II on the circadian variation of blood pressure. Furthermore, these data indicate that a permanent deficiency in the brain renin-angiotensin system alters the reflex control of heart rate in rats.
为研究脑肾素-血管紧张素系统是否在血压和心率变异性的长期及短期调控中发挥作用,我们检测了脑内血管紧张素原水平较低的转基因大鼠[TGR(ASrAOGEN)]的血压和心率24小时变化情况。在通过皮下低剂量输注血管紧张素II诱导7天的基础状态和高血压状态下进行遥测记录。通过频谱分析评估短期血压和心率变异性,并计算压力和心率变化之间的平均传递增益作为压力反射敏感性的指标。在血管紧张素II输注期间,对照大鼠而非TGR(ASrAOGEN)大鼠的血压24小时节律发生倒置(血压昼夜差异分别为5.8±2与-0.4±1.8 mmHg/组,P<0.05)。在对照大鼠和TGR(ASrAOGEN)大鼠中,心率的24小时节律均未改变,且与运动活动节律平行。在基础状态下,TGR(ASrAOGEN)大鼠0.3至0.6 Hz之间的传递增益显著高于对照大鼠(0.71±0.1与0.35±0.06,P<0.05),但在血管紧张素II输注期间无显著差异(0.6±0.07与0.4±0.1,P>0.05)。这些结果表明,脑肾素-血管紧张素系统在介导血管紧张素II对血压昼夜变化的影响中起重要作用。此外,这些数据表明脑肾素-血管紧张素系统的永久性缺陷会改变大鼠心率的反射性调控。