Berkowitz B A, Sherman S
J Pharmacol Exp Ther. 1982 Feb;220(2):329-34.
Vasopressin produced analgesia in mice as estimated by using abdominal constriction tests (ED50 8.5 micrograms/kg i.v.) or hot plate method (ED50 63 micrograms/kg i.v.). However, vasopressin (10 micrograms/kg i.v.) produced no depression of locomotor activity in mice. Vasotocin had slight analgesic action; oxytocin or norepinephrine had none and there was no direct correlation between pressor response and analgesia. The analgesic action was nonopiate in nature as it was uninfluenced by the narcotic antagonist naltrexone at 5 to 15 mg/kg, but it was reserved by a vasopressin antagonist. Intraventricular administration of vasopressin (1-10 micrograms/kg) to mice produced no significant analgesia, suggesting a primarily peripheral locus of analgesic action. Vasopressin may play a role as an endogeneous pain regulating substance.
通过腹部收缩试验(静脉注射半数有效量8.5微克/千克)或热板法(静脉注射半数有效量63微克/千克)评估,血管加压素可使小鼠产生镇痛作用。然而,血管加压素(静脉注射10微克/千克)对小鼠的运动活性并无抑制作用。催血压素具有轻微的镇痛作用;催产素或去甲肾上腺素则无此作用,且升压反应与镇痛之间无直接关联。该镇痛作用本质上是非阿片样的,因为在5至15毫克/千克剂量下,麻醉拮抗剂纳曲酮对其无影响,但血管加压素拮抗剂可逆转此作用。向小鼠脑室内注射血管加压素(1 - 10微克/千克)未产生明显镇痛作用,提示镇痛作用主要在外周部位。血管加压素可能作为一种内源性疼痛调节物质发挥作用。