Muscarinic modulation of acetylcholine release evoked by dimethylphenylpiperazinium and high potassium from guinea-pig myenteric plexus.
The effects of oxotremorine and atropine on the ACh release evoked from the guinea-pig myenteric plexus by dimethylphenylpiperazinium (DMPP) or by high potassium were investigated. DMPP caused an output of ACh by stimulating nicotine receptors that are probably situated on the soma-dendritic part of the cholinergic neuron. The DMPP-induced release of ACh was dose-dependently inhibited by oxotremorine and increased by atropine. The ACh output evoked by either 45 or 108 mM potassium was enhanced by atropine. Oxotremorine did not affect the ACh release by high potassium but prevented the facilitatory effect of atropine. It is concluded that the inhibitory muscarinic mechanism modulates similarly the ACh release evoked by DMPP or high potassium and the release caused by electrical stimulation. From the experiments with high potassium it is concluded that the inhibitory muscarine receptors are localized at the site of ACh release.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D001285:Atropine / Q000494:pharmacology; D004246:Dimethylphenylpiperazinium Iodide / Q000494:pharmacology*; D004347:Drug Interactions; D005260:Female; D006168:Guinea Pigs; D006584:Hexamethonium Compounds / Q000494:pharmacology; D066298:In Vitro Techniques; D008297:Male; D009197:Myenteric Plexus / Q000187:drug effects / Q000378:metabolism*; D010095:Oxotremorine / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology*; D011188:Potassium / Q000494:pharmacology*; D011950:Receptors, Cholinergic / Q000502:physiology*; D011976:Receptors, Muscarinic / Q000502:physiology*; D013779:Tetrodotoxin / Q000494:pharmacology
D006584:Hexamethonium Compounds; D010879:Piperazines; D011950:Receptors, Cholinergic; D011976:Receptors, Muscarinic; D013779:Tetrodotoxin; D004246:Dimethylphenylpiperazinium Iodide; D010095:Oxotremorine; D001285:Atropine; D000109:Acetylcholine; D011188:Potassium