Acute effects of N-methyl-N'-nitro-N-nitrosoguanidine on canine gastric mucosa.
The electrophysiological effects of the chemical gastric carcinogen N-methyl-N'-nitro-N-nitrosoquanidine (MNNG) were determined in an in vivo chambered canine stomach and in an in vitro canine gastric mucosal preparation. In the in vivo stomach, the topical application of 2.5 mg MNNG/ml decreased the transmural electrical potential difference, and the systemic blood pressure was essentially unchanged. In the in vitro preparation, exposure of the mucosal side of the isolated canine gastric mucosa to 0.25 and 2.5 mg MNNG/ml for 1 hour sequentially or exposure of the serosal side to 2.5 mg MNNG/ml for 2 hours inhibited net Na+ and Cl- fluxes. With longer duration, the undirectional fluxes of Na+ and Cl- increased, indicating an increase in permeability. These findings suggested that inhibition of active transport in the gastric mucosa may have an important function in the gastric carcinogenicity of MNNG.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002463:Cell Membrane Permeability / Q000187:drug effects; D002712:Chlorides / Q000378:metabolism; D004285:Dogs; D005260:Female; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism / Q000503:physiopathology; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects*; D008769:Methylnitronitrosoguanidine / Q000494:pharmacology*; D009374:Neoplasms, Experimental / Q000139:chemically induced; D012964:Sodium / Q000378:metabolism; D013274:Stomach Neoplasms / Q000139:chemically induced
D002712:Chlorides; D008769:Methylnitronitrosoguanidine; D012964:Sodium