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The inhibitory mechanism of GLP-1, but not glucagon, on fasted gut motility is dependent on the L-arginine/nitric oxide pathway.

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Animals, Arginine, metabolism, Dose-Response Relationship, Drug, Enzyme Inhibitors, pharmacology, Fasting, Gastrointestinal Motility, drug effects, physiology, Glucagon, Glucagon-Like Peptide 1, Male, Myoelectric Complex, Migrating, Nitric Oxide, Nitroarginine, Peptide Fragments, Protein Precursors, Rats, Sprague-Dawley, Rats

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      Abstract

      Effects of glucagon-like peptide-1 (GLP-1) and glucagon on fasted gut motility in conscious rats were investigated as regards dependence on nitric oxide (NO). Small bowel motility was studied by electromyography and a jugular vein catheter was implanted for administration of drugs. GLP-1 (5-40 pmol x kg(-1) x min(-1)) prolonged the cycle length and abolished phase III of the migrating myoelectric complex (MMC) (P<0.01). Low doses of GLP-1 did not affect duration, propagation velocity or calculated length of phase III. At 1 mg x kg(-1) N(omega)-nitro-L-arginine (L-NNA) blocked the GLP-1 response up to a dose of 10 pmol x kg(-1) x min(-1) (P<0.05), while higher doses were able to overcome L-NNA-induced disinhibition of the GLP-1 response (P<0.05). Similarly, L-arginine at 300 mg x kg(-1) prevented L-NNA-induced disinhibition of the GLP-1 response (P<0.05). Glucagon (200-1000 pmol x kg(-1) x min(-1)) prolonged the cycle length and abolished phase III of MMC (P<0.01) independent of NO. Again, low doses of glucagon did not affect duration, propagation velocity or calculated length of phase III. In conclusion, inhibition of fasted motility by GLP-1 at low doses is dependent on NO, while high doses of GLP-1 and glucagon exert effects on motility independently from NO.

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