In newborn infants, laryngeal contact with solutions of low chloride concentration or pH evokes swallowing, laryngeal adduction, and respiratory inhibition (laryngeal chemoreflex). To determine whether the laryngeal chemoreflex is present during fetal life and its effect on fetal respiratory activity, eight time-bred ewes (128 +/- 2 days) were prepared with fetal electrocortical diaphragm and esophageal electrodes and a nasopharyngeal catheter. After a 60-minute control period, increasing volumes (0.1 to 1.0 ml/kg) of 0.15 mol/L NaCl or distilled water (0.05 to 1.0 ml/kg) and decreasing concentrations of NaCl (0.15 to 0.02 mol/L) at a fixed volume (0.3 ml/kg) were sequentially administered through the nasopharyngeal catheter (38 degrees C). The minimum water volume that stimulated swallowing was significantly less than the minimum 0.15 mol/L NaCl volume (0.10 +/- 0.02 vs. 0.70 +/- 0.05 ml/kg). The maximum NaCl concentration that stimulated swallowing was 0.04 +/- 0.01 mol/L During the control period, respiratory activity averaged 14.6 +/- 0.7 breaths/minute and did not change during absent swallow responses or isotonic saline-induced swallows. However, respiratory activity significantly decreased during water (4.7 +/- 0.6 breaths/minute) and hypotonic saline-induced swallow responses (3.7 +/- 0.7 breaths/minute). Fetal electrocortical activity did not change during absent or stimulated swallows. We conclude that laryngeal water or hypotonic saline solution may stimulate fetal swallowing and suppress fetal respiratory activity, similar to the newborn laryngeal chemoreflex. We speculate that an exaggeration of the laryngeal chemoreflex apnea response in the newborn may predispose to sudden infant death syndrome.