Nociceptive inhibition of migrating myoelectric complex by nitric oxide and monoaminergic pathways in the rat

Abstract

This study investigated the role of nitric oxide (NO) and adrenergic and dopaminergic mechanisms in reflex inhibition of the migrating myoelectric complex (MMC) after intraperitoneal administration of acid in rats. 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 Nω-nitro-l-arginine, reserpine, or guanetidine before acid decreased the prolonged cycle length to 18.1 ± 2.8 ( P < 0.001), 19.0 ± 2.0 ( P < 0.001), and 27.5 ± 9.3 min ( P < 0.001), respectively. Similarly, haloperidol given 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 propranolol or hexamethonium given alone. After intraperitoneal instillation of acid there was an increase in the plasma levels of somatostatin 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 adrenergic, dopaminergic, and somatostatinergic mechanisms cooperate in inhibiting the MMC after nociceptive stimulation of the peritoneum.