Add time:08/07/2019         Source:sciencedirect.com

The effect of fedotozine (cas 123618-00-8) on visceral hypersensitivity was evaluated in conscious rats. One hour after colonic irritation (0.6% acetic acid intracolonically), a 30 mmHg colonic distension was applied for 10 min. Irritation increased the number of abdominal contractions induced by colonic distension (23.4±4.1 versus 4.8±1.4 in saline-treated rats, P<0.001). Facilitation of colonic pain was reversed in a dose-dependent manner by fedotozine ((+)-(-1R)-1-phenyl-1-[(3,4,5-trimethoxy)benzyloxymethyl]-N,N-dimethyl-n-propylamine), (±)-U-50,488H (trans-(±)-3,4-dichloro-N-methyl-N-(2-[1-pyrrolidinyl]cyclohexyl)benzeneacetamide) and morphine (respective ED50 values 0.67, 0.51 and 0.23 mg/kg s.c.). The κ-opioid receptor antagonist, nor-binaltorphimine, abolished the effects of fedotozine and (±)-U-50,488H but not those of morphine. Low doses of naloxone (30 μg/kg s.c.) blocked the effect of morphine but not of fedotozine or (±)-U-50,488H. After intracerebroventricular administration, morphine was very potent (ED50 1.7 μg/rat), (±)-U-50,488H poorly active (58% of antinociception at 300 μg/rat) and fedotozine inactive up to 300 μg/rat. These results show that fedotozine blocks hypersensitive visceral pain by acting on peripheral κ-opioid receptors in animals. © 1997 Elsevier Science B.V.

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