The balloon distension (BD)-induced descending peristaltic reflex in the opossum smooth muscle esophagus is abolished in vitro when a Ca(2+)-free Krebs solution is placed at the site of distension, suggesting that either synaptic transmission occurs at the origin of the reflex or initiation of the reflex requires the development of muscle tension in response to BD. To test the latter possibility, an 8- to 10-cm length of smooth muscle esophagus was placed in a dual-chamber organ bath, isolating the stimulating (orad) from the recording site (aborad). Nifedipine addition to the orad chamber (i.e., site of distension) inhibited the BD-induced "off" contractions in both chambers in a concentration-dependent manner. However, the aborad response to electrical field stimulation (EFS) was unaffected. Atropine addition to the orad chamber had no effect on BD or EFS responses in either chamber. To examine the effects of these agents on tonic contractility, an isobaric barostat was employed. Pressure-volume curves were not altered by Ca(2+)-free Krebs solution, nifedipine, or TTX, suggesting that resting esophageal tone is not dependent on neural factors or muscle contractility. However, both Ca(2+)-free Krebs solution and nifedipine markedly decreased phasic contractions over the top of the distending bag. These observations suggest that local, stretch-induced phasic muscle contraction is required for initiation of the BD-induced descending peristaltic reflex.