NOCICEPTIVE INHIBITION OF MIGRATING MYOELECTRIC COMPLEX BY NITRIC-OXIDE AND MONOAMINERGIC PATHWAYS IN THE RAT

This study investigated the role of nitric oxide (NO) and adrenergic a nd dopaminergic mechanisms in reflex inhibition of the migrating myoel ectric complex (MMC) after intraperitoneal administration of acid in r ats. Acid instilled immediately after an activity front inhibited the migrating complex and prolonged the cycle length from 13.0 +/- 0.7 to 98.5 +/- 17.2 min (P < 0.001). Administration of N-omega-nitro-L-argin ine, reserpine, or guanetidine before acid decreased the prolonged cyc le length to 18.1 +/- 2.8 (P < 0.001), 19.0 +/- 2.0 (P < 0.001), and 2 7.5 +/- 9.3 min (P < 0.001), respectively. Similarly, haloperidol give n before acid shortened the prolonged cycle length to 46.7 +/- 5.2 min (P < 0.05). There was no effect of phentolamine in combination with p ropranolol or hexamethonium given alone. After intraperitoneal instill ation of acid there was an increase in the plasma levels of somatostat in and a decrease of calcitonin gene-related peptide, but there was no change of neuropeptide Y, vasoactive intestinal peptide, substance P, neurokinin A, or neurotensin. The results indicate that NO and adrene rgic, dopaminergic, and somatostatinergic mechanisms cooperate in inhi biting the MMC after nociceptive stimulation of the peritoneum.