Gardiner S M, Bennett T
Medical School, Queen's Medical Centre, Nottingham, U.K.
J Auton Nerv Syst. 1988 Oct;24(3):193-203. doi: 10.1016/0165-1838(88)90119-1.
In conscious rats, in the presence of prazosin and idazoxan (alpha 1- and alpha 2-adrenoceptor antagonists, respectively), blood pressure (BP) and heart rate (HR) become unstable, due to the occurrence of 'spontaneous' depressor and tachycardic episodes. These events could be triggered also by auditory stimuli, and were blocked by antagonism of beta 2-adrenoceptors. In adrenal-demedullated animals treated with prazosin and idazoxan, BP was less variable than in sham-operated animals, but bolus injections of adrenaline or salbutamol could simulate the 'spontaneous' depressor events seen in the latter. The marked swings in HR were not explained by sensitization of the cardiac baroreflex in the presence of idazoxan, but were probably due to blockade of prejunctional autoinhibitory alpha 2-adrenoceptors, amplifying the effects of intermittent sympatho-adrenal activation.
在清醒大鼠中,在哌唑嗪和咪唑克生(分别为α1和α2肾上腺素能受体拮抗剂)存在的情况下,由于出现“自发性”降压和心动过速发作,血压(BP)和心率(HR)变得不稳定。这些事件也可由听觉刺激触发,并被β2肾上腺素能受体拮抗作用阻断。在用哌唑嗪和咪唑克生治疗的肾上腺髓质切除动物中,血压的变异性比假手术动物小,但静脉注射肾上腺素或沙丁胺醇可模拟后者出现的“自发性”降压事件。心率的显著波动不能用咪唑克生存在时心脏压力反射的敏化来解释,而可能是由于节前自身抑制性α2肾上腺素能受体被阻断,放大了间歇性交感-肾上腺激活的作用。