Journal Article

Effect of selective and non-selective muscarinic blockade on baclofen inhibition of gastric carcinogenesis induced by <i>N</i>-methyl-<i>N</i>'-nitro-<i>N</i>-nitrosoguanidine in Wistar rats

Masaharu Tatsuta, Hiroyasu Iishi, Miyako Baba, Hiroyuki Yano, Hiroyuki Uehara and Aklhiko Nakaizumi

in Carcinogenesis

Volume 17, issue 2, pages 293-296
Published in print February 1996 | ISSN: 0143-3334
Published online February 1996 | e-ISSN: 1460-2180 | DOI: http://dx.doi.org/10.1093/carcin/17.2.293
Effect of selective and non-selective muscarinic blockade on baclofen inhibition of gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine in Wistar rats

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The effects of baciofen, a γ-amino-n-butyic acid receptor B agonist, on gastric carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine and how its effects areinfluenced by selective (M1) and non-selective (M1 and M2) pharmacological blockade of muscarinic receptors were investigated in inbred Wistar rats. Rats were given s.c. injections of 8 mg/kg body wt baclofen with and without 0.5 mg/kg body wt atropine (non-selective M1 and M2 muscarinic receptorantagonist) or 1.0 mg/kg body wt pirenzepine (selective M1 muscarinic receptor antagonist every other day after a 25 week carcinogen treatment. At week 52 baclofen significantly decreased the incidence of gastric cancers. Concomitant treatment with atropine significantly attenuated the inhibition by baclofen of gastric carcinogenesis, but combined use with pirenzepine had no significant effect on the inhibition by baclofen of gastric carcinogenesis. Baclofen also significantly decreased the labeling index of the antralo mucosa. Baclofen plus atropine attenuated the decrease in the labeling index of the antral mucosa due to baclofen, but baclofen plus pirenzepine had no significant effect on the labeling index. These results suggest that the inhibition of gastric carcinogenesis by baclofen is medicated through muscarinic receptors and M2 receptors, but not M1 receptors, are involved in this response.

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Subjects: Clinical Cytogenetics and Molecular Genetics

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