CDP-choline-induced contractions in the mouse gastric fundus through purinoceptors and Rho/Rho-kinase signalling.

摘要: Abstract Aims This study aimed to investigate the effects of cytidine-5′-diphosphocholine (CDP-choline), an endogenous lipid precursor, on reactivity mouse gastric fundus and determine mechanism(s) mediating its effects. Main methods Possible contractile effect CDP-choline (10 − 5 –10 − 2  M) was investigated in absence presence a muscarinic receptor antagonist, atropine (3 × 10 − 6  M), acetylcholine esterase inhibitor, physostigmine Na + channel blocker, tetrodotoxin (TTX, 3 × 10 Rho-kinase Y-27632 M), purinoceptor suramin (2 × 10 − 4 nitric oxide synthase N G -nitro-L-arginine (L-NA, Ca 2+ nifedipine α 7 nicotinic methyllycaconitine citrate (MLA, 10 protein (G i/o ) pertussis toxin (PTX, 2 μg/ml). The metabolites CDP-choline, namely choline cytidine 5′-triphosphate (CTP, monophosphate (CMP, − 3 were also tested. Besides, phosphorylation MYPT1, which indicates activity, detected. Key findings produced contractions concentration-dependent manner. not affected by atropine, physostigmine, TTX, PTX, MLA or L-NA. However, Y-27632, partly reduced these contractions. increased MYPT1. Among metabolites, had no induced considerable contractions, sensitive atropine. CMP CTP comparable that CDP-choline. Significance These results suggest contraction through, at least part, purinoceptors Rho/Rho-kinase signalling fundus.