›› 2007, Vol. 27 ›› Issue (1): 25-28.

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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

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