Abdel-Rahman A A
Department of Pharmacology, East Carolina University School of Medicine, Greenville, NC 27858.
J Cardiovasc Pharmacol. 1992 Feb;19(2):233-45. doi: 10.1097/00005344-199202000-00012.
This study tested the hypothesis that aortic baroreceptors exert a central restraining influence on centrally mediated depressor responses and that this mechanism is tonically active and is independent of their modulation of basal arterial pressure. The effects of short-term (48-72 h) aortic baroreceptor deafferentation (ABD) on the acute hemodynamic (peripherally mediated pressor and centrally mediated depressor) effects of clonidine were investigated in conscious and anesthetized normotensive rats. ABD caused an immediate increase in basal arterial pressure and heart rate and a significant attenuation of the baroreceptor reflex control of heart rate. Since only arterial pressure subsided to control levels by 48-72 h, the data suggest that central reorganizational changes were potent enough to overcome the tonically active restraining influence of aortic baroreceptors on basal arterial pressure but not heart rate. Clonidine produced a similar pressor effect in conscious ABD and sham rats but its depressor effect was significantly greater in ABD rats whose baroreceptor reflex control of heart rate was significantly attenuated. Intracisternal (i.c.) administration of 0.1 microgram of clonidine, a dose that had no effect when administered i.v., produced a near-maximal depressor effect in conscious ABD rats vs. no effect in sham rats (-16.7 +/- 4.1 vs. -0.3 +/- 2 mm Hg; p less than 0.001). The depressor effect of clonidine was also enhanced in chloralose-anesthetized rats and coincided with an anesthesia-induced attenuation of the baroreceptor reflex control of heart rate. It is concluded that aortic baroreceptors exert a potent restraining influence on the centrally mediated depressor effect of clonidine. Since ABD had no significant effect on the depressor response to nitroprusside, but enhanced the depressor response to ganglion blockade by hexamethonium, the data suggest that a higher peripheral sympathetic neural activity existed in ABD rats. The reorganizational changes that occurred within 48-72 h after ABD were potent enough to overcome the tonically active restraining influence of aortic baroreceptors on basal arterial pressure but not on the centrally mediated depressor responses. Thus, the buffering influence of aortic baroreceptors and their central projections on centrally mediated depressor responses seems to be tonically involved in blood pressure control.
主动脉压力感受器对中枢介导的降压反应发挥中枢性抑制作用，且该机制持续活跃，独立于其对基础动脉血压的调节。在清醒和麻醉的正常血压大鼠中，研究了短期（48 - 72小时）主动脉压力感受器去传入（ABD）对可乐定急性血流动力学效应（外周介导的升压和中枢介导的降压）的影响。ABD导致基础动脉血压和心率立即升高，且压力感受器对心率的反射控制显著减弱。由于仅动脉血压在48 - 72小时后降至对照水平，数据表明中枢重组变化足以克服主动脉压力感受器对基础动脉血压的持续活跃抑制作用，但对心率无效。可乐定在清醒的ABD大鼠和假手术大鼠中产生相似的升压作用，但其降压作用在ABD大鼠中显著更大，其压力感受器对心率的反射控制显著减弱。脑池内（i.c.）给予0.1微克可乐定，该剂量静脉注射时无作用，但在清醒的ABD大鼠中产生接近最大的降压作用，而在假手术大鼠中无作用（-16.7±4.1对-0.3±2 mmHg；p＜0.001）。可乐定的降压作用在氯醛糖麻醉的大鼠中也增强，且与麻醉诱导的压力感受器对心率的反射控制减弱一致。结论是主动脉压力感受器对可乐定的中枢介导降压作用发挥强大的抑制作用。由于ABD对硝普钠的降压反应无显著影响，但增强了六甲铵对神经节阻断的降压反应，数据表明ABD大鼠存在较高的外周交感神经活动。ABD后48 - 72小时内发生的重组变化足以克服主动脉压力感受器对基础动脉血压的持续活跃抑制作用，但对中枢介导的降压反应无效。因此，主动脉压力感受器及其中枢投射对中枢介导降压反应的缓冲影响似乎持续参与血压控制。
