Evidence for a peripheral mechanism of esophagocrural diaphragm inhibitoryreflex in cats

The esophagogastric junction (EGJ) is guarded by two sphincters, a smooth m uscle lower esophageal sphincter (LES) and a skeletal muscle crural diaphra gm. These two sphincters relax simultaneously under certain physiological c onditions, i.e., swallowing, belching, vomiting, transient LES relaxation, and esophageal distension. Esophageal distension-induced crural diaphragm r elaxation is mediated through vagal afferents that are thought to exert inh ibitory influence on the central mechanism (brain stem) of crural diaphragm contraction. We conducted studies in 10 cats to determine whether a mechan ism of crural diaphragm relaxation was located at the level of the neuromus cular junction and/or muscle. Stimulation of the crural diaphragm neuromusc ular junction through 1) the electrodes implanted in the muscle and 2) the bilateral phrenic nerve resulted in an increase in EGJ pressure. Nicotinic receptor blockade (pancuronium, 0.2 mg/kg) abolished the EGJ pressure incre ase caused by electrical stimulation of the neuromuscular junction. Esophag eal distension and bolus-induced secondary esophageal peristalsis caused re laxation of the EGJ during the stimulation of the neuromuscular junction. B ilateral phrenicotomy and vagotomy had no influence on this relaxation. The se data suggest the existence of a peripheral mechanism of crural diaphragm inhibition. This peripheral inhibitory mechanism may reside at the level o f either the neuromuscular junction or the skeletal muscle.