›› 2007, Vol. 27 ›› Issue (1): 25-28.

• 论文 • 上一篇    下一篇

外周α1和α2受体参与应激性高血压对大鼠颈动脉窦反射的抑制

  

  1. 苏州大学医学院基础医学系生理学教研室,苏州 215123
  • 收稿日期:2006-07-19 出版日期:2007-01-31 发布日期:2007-01-31
  • 基金资助:
    苏州大学医学院科学技术项目(编号:1995A-1)

Peripheral α1 and α1 Receptors Involved in Stressful Hypertension -Induced Inhibition of Carotid Sinus Baroreceptor Reflex in Rats

  1. Department of Physiology, Medical School of Soochow University, Suzhou 215123, China
  • Received:2006-07-19 Online:2007-01-31 Published:2007-01-31

摘要: 目的 探讨外周α1和α2受体是否参与应激性高血压对颈动脉窦反射(CSR)的重调定.方法 应激一周的雄性SD大鼠,麻醉后孤离双侧颈动脉窦区,将不同窦内压(ISP)与其对应的平均动脉压(MAP)值进行Logistic五参数曲线方程拟合,求得ISP-MAP关系曲线及特征参数,观察外周静脉注射(iv.)选择性α1或α2受体拮抗剂酚苄明(PBZ)或育亨宾(YOH)对应激性CSR的影响.结果 iv.PBZ(2.5 μmol/L,0.15μl/g)导致应激大鼠ISP-MAP关系曲线显著下移(P<0.05),反射参数中阈压、饱和压和最大增益时的窦内压值减小(P<0.05),而最大增益加大(P<0.05);iv.YOH(5μmol/L,0.15μl/g)对应激性高血压所致ISP-MAP关系曲线及其反射参数效应的影响,与iv.PBZ后的相类似,但YOH的作用不如PBZ的明显(P<0.05);iv.相应剂量的PBZ或YOH对非应激大鼠的CSR无明显影响(P>0.05);iv.PBZ或YOH均不能使应激的CSR水平恢复到相应的非应激给药后水平.结论 外周α1、α2受体参与应激性高血压对CSR的抑制性重调定;外周α1受体在这种重调定的机制中可能发挥更为重要的作用;此外,应激性高血压对CSR的作用中尚有其他因素的参与.

关键词: 颈动脉窦反射, 应激性高血压, 外周α1受体, 外周α2受体, 平均动脉压, 大鼠

Abstract: Objective To investigate the effects of peripheral oti and Ol2 receptors on the stressful hypertension-induced carotid sinus baroreceptor reflex (CSR) resetting. Methods Twenty-three male Sprague-Dawley rats were subjected to unavoidable electric foot-shock twice daily for a week, each session of foot-shock lasted 2 hours. The left and right carotid sinus regions were isolated from the systemic circulation under anesthesia with pentobarbital sodium. The intracarotid sinus pressure (ISP) was altered in a stepwise manner in vivo. ISP- mean arterial pressure (MAP) relationship curve and its characteristic parameters were constructed by fitting to the logistic function with five parameters. We observed the changes in CSR performance resulted from stressful hypertension and the effects of injection with Ol1 or Ol2 receptor selective antagonist, phenoxybenzamine (PBZ) or yohimbine (YOH), into the peripheral vein on the responses of CSR to stressful hypertension. Results Peripheral veinal injection (iv.) of PBZ (2.5 jumol/L, in 0.15 jul/g) significantly shifted the ISP-MAP relationship curve downwards (P</i><0.05) and obviously decreased the value of the reflex parameters such as threshold pressure, saturation pressure and ISP at maximum gain (P<0.05), but increased maximum gain (P<0.05) in the stressed rats. The effects of iv. YOH (5 jumol/L, in 0.15 ul/g) on the changes in CSR induced by stressful hypertension were similar to those of PBZ, but the effect of YOH was less remarkable than that of PBZ (P<0.05). Peripheral injection with the corresponding dose of PBZ or YOH in the unstressed rats did not change CSR performance significantly (P</i>>0.05). However, injection of PBZ or YOH could not completely abolish the stressful hypertension-induced changes in CSR performance. Conclusion Peripheral oti and (Ol2 receptors are involved in the stressful hypertension-induced CSR inhibitory resetting. Peripheral Ol1 receptor may play more important roles in this resetting and at the same time, the effects of stressful hypertension on CSR also have other mechanism.

Key words: Carotid sinus baroreceptor reflex, Stressful hypertension, Peripheral oti receptor,Peripheral Ol2 receptor, Mean arterial pressure, Rat