To evaluate the mechanism of gastric adaptive relaxation (GAR), we designed and established the experimental system for the measurement of GAR in isolated stomach from the guinea-pig by modifying the method of Desai. We also investigated the roles of non-adrenergic, non-cholinergic (NANC) nerves and endogenous nitric oxide (NO) in GAR by using this system. The rapid increase in the capacity of isolated stomach was observed over a certain pressure as GAR. GAR was abolished by tetrodotoxin (10(-6) M) in the presence of atropine (3 x 10(-6) M) and guanethidine (5 x 10(-6) M). NG-nitro L-arginine (LNNA) (10(-4) M), a NO synthesis inhibitor, also abolished GAR. L-arginine (10(-3) M), a precursor for NO synthesis, reversed LNNA-induced impairment of GAR. Sodium nitroprusside (10(-6)-10(-4) M), a NO-donor, induced the gastric relaxation. These results suggest that GAR is mediated by NANC nerves, possibly via endogenous NO.
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