Sakitama K
Pharmacology Section, Nippon Kayaku Co., Ltd., Tokyo, Japan.
Jpn J Pharmacol. 1993 Jun;62(2):131-6. doi: 10.1254/jjp.62.131.
The effects of intrathecal noradrenaline (NA) on the flexor reflex mediated by group II afferent fibers (group II flexor reflex) were investigated in anesthetized spinal rats. Low doses (0.01 and 0.1 mumol) of NA-HCl inhibited the group II flexor reflex, while high doses (1 and 10 mumol) facilitated it. In rats pretreated with the selective alpha 2-antagonist yohimbine-HCl (0.1 mumol), the effect of NA-HCl (0.1 mumol) shifted from inhibition to facilitation. Intravenous administration of prazosin-HCl (0.1 and 1 mg/kg, i.v.), a selective alpha 1-antagonist, dose-dependently antagonized the facilitation of the group II flexor reflex induced by NA-HCl in rats pretreated with yohimbine-HCl. The selective alpha 1-agonist methoxamine-HCl (1 mumol) and the alpha 2-agonist clonidine-HCl (0.1 mumol) facilitated and inhibited the group II flexor reflex, respectively. The effects of clonidine-HCl and methoxamine-HCl were almost the same as those of NA-HCl at doses of 0.1 and 10 mumol, respectively. NA-HCl (1 and 10 mumol) and methoxamine-HCl (1 mumol) increased the spontaneous electromyogram (EMG) spikes of the muscle tibialis anterior. The time course of the increase in the spontaneous EMG spikes was similar to that observed in the group II flexor reflex. These results suggest that NA facilitates and inhibits the group II flexor reflex via alpha 1- and alpha 2-receptors, respectively, and one of the mechanisms of the facilitatory effects is the elevation of excitability of the alpha-motoneuron.
在麻醉的脊髓大鼠中，研究了鞘内注射去甲肾上腺素（NA）对由II类传入纤维介导的屈肌反射（II类屈肌反射）的影响。低剂量（0.01和0.1 μmol）的盐酸去甲肾上腺素抑制II类屈肌反射，而高剂量（1和10 μmol）则促进该反射。在用选择性α2拮抗剂盐酸育亨宾（0.1 μmol）预处理的大鼠中，盐酸去甲肾上腺素（0.1 μmol）的作用从抑制转变为促进。静脉注射选择性α1拮抗剂盐酸哌唑嗪（0.1和1 mg/kg，静脉注射），剂量依赖性地拮抗了在用盐酸育亨宾预处理的大鼠中由盐酸去甲肾上腺素诱导的II类屈肌反射的促进作用。选择性α1激动剂盐酸甲氧明（1 μmol）和α2激动剂盐酸可乐定（0.1 μmol）分别促进和抑制II类屈肌反射。盐酸可乐定和盐酸甲氧明的作用分别与0.1和10 μmol剂量的盐酸去甲肾上腺素的作用几乎相同。盐酸去甲肾上腺素（1和10 μmol）和盐酸甲氧明（1 μmol）增加了胫前肌的自发电活动（EMG）峰值。自发电活动峰值增加的时间进程与在II类屈肌反射中观察到的相似。这些结果表明，NA分别通过α1和α2受体促进和抑制II类屈肌反射，促进作用的机制之一是α运动神经元兴奋性的升高。
