Harris J, Clarke R W
Department of Physiology and Environmental Science, University of Nottingham, Loughborough, Leicestershire, UK.
Exp Brain Res. 1992;92(2):310-7. doi: 10.1007/BF00227973.
The sural-gastrocnemius reflex was observed in decerebrated rabbits during intrathecal application of four alpha-adrenoceptor antagonists. Idazoxan and yohimbine, which are antagonists at the alpha 2-receptor, caused facilitation of the reflex, although idazoxan was more potent and produced a larger overall increase in the reflex response. However, when given after yohimbine, idazoxan elicited no further increase in reflex responses. The differences between the two drugs may result from the interaction of yohimbine with receptors for 5-hydroxytryptamine. The selective alpha 1-receptor antagonist prazosin had no consistent effects when given alone, but reduced the facilitatory effects of idazoxan. The putative selective post-junctional alpha 2-receptor blocker SK&F 104078 had no significant effects when given alone, nor did it influence the facilitatory action of a subsequent dose of idazoxan. Section of the spinal cord in the presence of idazoxan always caused a decrease in gastrocnemius responses to sural nerve stimulation. These data show that the facilitatory effects of idazoxan are almost certainly mediated at the spinal cord and that they do not involve blockade of alpha 1-receptors. It appears that idazoxan acts by blockade of adrenergic descending inhibition in combination with increased descending facilitation. The inhibition is probably mediated through noradrenaline acting at alpha 2-receptors, and the facilitation may be the result of release of noradrenaline (acting at alpha 1-receptors) and 5-hydroxytryptamine in the spinal cord.
在鞘内应用四种α-肾上腺素能受体拮抗剂期间,观察了去大脑家兔的腓肠肌-比目鱼肌反射。α₂受体拮抗剂咪唑克生和育亨宾可使反射增强,尽管咪唑克生作用更强,使反射反应的总体增幅更大。然而,在育亨宾给药后再给予咪唑克生时,反射反应并未进一步增强。这两种药物之间的差异可能是由于育亨宾与5-羟色胺受体相互作用所致。选择性α₁受体拮抗剂哌唑嗪单独给药时没有一致的效应,但可减弱咪唑克生的增强作用。假定的选择性节后α₂受体阻滞剂SK&F 104078单独给药时无显著效应,也不影响随后给予的咪唑克生的增强作用。在存在咪唑克生的情况下切断脊髓,总是会导致比目鱼肌对腓肠神经刺激的反应减弱。这些数据表明,咪唑克生的增强作用几乎肯定是在脊髓介导的,且不涉及α₁受体的阻断。似乎咪唑克生通过阻断肾上腺素能下行抑制并结合增强下行易化作用来发挥作用。这种抑制可能是通过去甲肾上腺素作用于α₂受体介导的,而这种易化作用可能是脊髓中去甲肾上腺素(作用于α₁受体)和5-羟色胺释放的结果。