In many species submucosal glands are an important source of tracheal mucus, but the extent to which mucociliary clearance (MCC) depends upon gland secretion is unknown. To explore this relationship, we measured basal and agonist-stimulated MCC velocities in ex-vivo tracheas from adult ferrets and compared the velocities with previously measured rates of ferret glandular mucus secretion (Cho, et al. AJP Lung, 2010, 299, L124). Stimulated MCC velocities (mm•min-1, mean ± SE for 10-35 min period post-stimulation) were as follows: 1 μM Carbachol: 19.1±3.3 > 10 μM phenylephrine: 15.3±2.4 10 μM isoproterenol: 15.0±1.9 10 μM forskolin: 14.6±3.1 > 1 μM VIP: 10.2±2.2 >> basal (t₁₅): 1.8 ± 0.3, n = 5-10 for each condition. Synergistic stimulation of MCC was observed between low concentrations of carbachol (100 nM) and isoproterenol (300 nM). Bumetanide inhibited carbachol-stimulated MCC by ~70%, and abolished the increase in MCC stimulated by forskolin + VIP, whereas HCO₃^--free solutions did not significantly inhibit MCC to either [Ca²⁺]_i or [cAMP]_i -elevating agonists. Stimulation and inhibition of MCC and gland secretion differed in several respects: most importantly, elevating [cAMP]_i increased MCC much more effectively than expected from its effects on gland secretion; and bumetanide almost completely inhibited [cAMP]_i -stimulated MCC while it has a smaller effect on gland secretion. We conclude that changes in glandular fluid secretion are complexly related to MCC and discuss possible reasons for this.