Kontani H, Maruyama I, Sakai T
Department of Pharmacology, Hokuriku University, School of Pharmacy, Kanazawa, Japan.
Jpn J Pharmacol. 1992 Dec;60(4):363-8. doi: 10.1254/jjp.60.363.
We have studied the effects of intrathecally-injected drugs that act on alpha-adrenoceptors in the urinary bladder reflex contractile activity evoked by continuous infusion of fluid into the bladder of anesthetized rats. Clonidine (10 and 30 micrograms) facilitated and yohimbine (100 micrograms) abolished the bladder contractile activity, and pretreatment with yohimbine (30 micrograms) inhibited the effect of clonidine (10 micrograms). Phenylephrine (60 micrograms) abolished the bladder contractile activity, but prazosin (40 micrograms) had no significant effect on it. The bladder contractions induced by electrical stimulation of the pontine micturition center were inhibited by yohimbine in a dose-dependent manner. These results suggest that transmission in the descending neurons from the pontine micturition center to the sacral parasympathetic neurons that control bladder motility is mediated by alpha 2-adrenoceptors in rats.
我们研究了鞘内注射作用于α-肾上腺素能受体的药物对麻醉大鼠膀胱持续输注液体诱发的膀胱反射性收缩活动的影响。可乐定(10微克和30微克)促进膀胱收缩活动,育亨宾(100微克)则消除膀胱收缩活动,预先给予育亨宾(30微克)可抑制可乐定(10微克)的作用。去氧肾上腺素(60微克)消除膀胱收缩活动,但哌唑嗪(40微克)对其无显著影响。育亨宾以剂量依赖的方式抑制电刺激脑桥排尿中枢诱发的膀胱收缩。这些结果表明,在大鼠中,从脑桥排尿中枢到控制膀胱运动的骶副交感神经元的下行神经元传递是由α2-肾上腺素能受体介导的。