We studied pressure-flow relationships in the supraglottic airway of eight prone mouth-open anesthetized (intravenous chloralose or pentobarbital sodium) crossbred dogs (weight 15-26 kg) during increasing respiratory drive (CO2 administration; n = 4) and during graded-voltage electrical stimulation (SV; n = 4) of the soft palate muscles. During increased respiratory drive, inspiratory airflow occurred via both the nose (Vn) and mouth (Vm), with the ratio of Vn to Vm [%(Vn/Vm)] decreasing maximally from 16.0 +/- 7.0 (SD) to 2.4 +/- 1.6% (P < 0.05). Simultaneously, oral airway resistance at peak inspiratory flow decreased from 2.1 +/- 1.0 to 0.4 +/- 0.4 cmH2O (P < 0.05), whereas nasal airway resistance did not change (14.4 +/- 7.2 to 13.1 +/- 5.4 cmH2O; P = 0.29). Inspiratory pressure-flow plots of the oral airway were inversely curvilinear or more complex in nature. Nasal pathway plots, however, demonstrated a positive linear relationship in all animals (r = 0.87 +/- 0.11; all P < 0.001). During electrical stimulation of soft palate muscle contraction accompanied by graded constant-inspiratory airflows of 45-385 ml/s through an isolated upper airway, %(Vn/Vm) decreased from 69 +/- 50 to 10 +/- 13% at a SV of 84 +/- 3% of maximal SV (P < 0.001). At a SV of 85 +/- 1% of maximum, normalized oral airway resistance (expressed as percent baseline) fell to 5 +/- 3%, whereas normalized nasal resistance was 80 +/- 9% (both P < 0.03). Thus control of oronasal airflow partitioning in dogs appears mediated more by alterations in oral route geometry than by closure of the nasopharyngeal airway.