Tank Jens, Jordan Jens, Diedrich André, Obst Michael, Plehm Ralph, Luft Friedrich C, Gross Volkmar
Department of Nephrology and Hypertension, Franz-Volhard-Clinic, Medical Faculty of the Charité and HELIOS Klinikum, Berlin, Germany.
Hypertension. 2004 May;43(5):1042-7. doi: 10.1161/01.HYP.0000125884.49812.72. Epub 2004 Mar 29.
Alpha-2 adrenoceptors are important in baroreflex regulation. We tested the impact of alpha-2 adrenoceptors on heart rate variability (HRV) and spontaneous baroreflex sensitivity (BRS) in conscious mice with telemetry (TA11PA-C20). Baseline beat-to-beat measurements (2 hours between 8:00 am to 12:00 pm) were compared with measurements after intraperitoneal alpha-2 adrenoceptor blockade (yohimbine 2 mg/kg) and alpha-2 adrenoceptor stimulation (clonidine 1, 10, and 50 mg/kg). Blood pressure (BP) was 128+/-6/87+/-6 mm Hg and heart rate (HR) was 548+/-18 bpm at baseline. BRS, calculated with the cross-spectral method, was 1.2+/-0.1 ms/mm Hg at baseline. BP increased 20+/-2/13+/-2 mm Hg with yohimbine. HR increased by 158+/-23 bpm. BRS did not change. BP decreased 16+/-7/5+/-4 mm Hg with 1 mg/kg of clonidine and did not change with a higher dose. HR decreased with clonidine (176+/-28, 351+/-21, 310+/-29 bpm during 1, 10, and 50 mg/kg of clonidine, P<0.01). HRV (total power=4629+/-465, 7002+/-440, and 6452+/-341 ms2 during 1, 10, and 50 mg/kg of clonidine, P<0.01) and BRS were profoundly increased with clonidine (14+/-1, 13+/-1, and 10+/-1 ms/mm Hg, P<0.01). The effects of clonidine were abolished with atropine (2 mg/kg plus 50 mg/kg of clonidine) but not with metoprolol (4 mg/kg plus 50 mg/kg of clonidine). These data suggest that alpha-2 adrenoceptors exert a regulatory influence on autonomic cardiovascular control and baroreflex function. The effect of clonidine on baroreflex HR regulation is mediated by the parasympathetic nervous system. These murine data fit well with recent human observations regarding parasympathetic activation via alpha-2 adrenoceptors.
α-2肾上腺素能受体在压力反射调节中起重要作用。我们使用遥测技术（TA11PA-C20）测试了α-2肾上腺素能受体对清醒小鼠心率变异性（HRV）和自发性压力反射敏感性（BRS）的影响。将基线逐搏测量值（上午8:00至12:00之间的2小时）与腹腔注射α-2肾上腺素能受体阻滞剂（育亨宾2mg/kg）和α-2肾上腺素能受体激动剂（可乐定1、10和50mg/kg）后的测量值进行比较。基线时血压（BP）为128±6/87±6mmHg，心率（HR）为548±18次/分钟。用互谱法计算的BRS在基线时为1.2±0.1ms/mmHg。育亨宾使BP升高20±2/13±2mmHg，HR增加158±23次/分钟，BRS未改变。1mg/kg可乐定使BP降低16±7/5±4mmHg，更高剂量时BP未改变。可乐定使HR降低（1、10和50mg/kg可乐定期间分别为176±28、351±21、310±29次/分钟，P<0.01）。可乐定使HRV（1、10和50mg/kg可乐定期间总功率分别为4629±465、7002±440和6452±341ms2，P<0.01）和BRS显著增加（分别为14±1、13±1和10±1ms/mmHg，P<0.01）。可乐定的作用可被阿托品（2mg/kg加50mg/kg可乐定）消除，但不能被美托洛尔（4mg/kg加50mg/kg可乐定）消除。这些数据表明，α-2肾上腺素能受体对自主心血管控制和压力反射功能发挥调节作用。可乐定对压力反射性心率调节的作用由副交感神经系统介导。这些小鼠数据与最近关于通过α-2肾上腺素能受体激活副交感神经的人体观察结果非常吻合。
