Mechanisms of saliva formation by wombat parotid glands were investigated in anaesthetized wombats at two levels of cholinergically-stimulated flow viz. mid-range (30-40% maximum flow) and maximum flow using ion-transport and carbonic-anhydrase inhibitors. Bumetanide (0.005-0.1mmoll-1 carotid plasma) progressively reduced mid-range flow by 52 ± 3.4% (mean ± SEM). Concurrently, saliva [Cl] decreased, [Na] and [HCO3] increased but HCO3 excretion was unaltered. Salivary flow during high-rate cholinergic stimulation was 31 ± 1.1% of the pre-bumetanide maximum. During mid-range stimulation, SITS (0.075mmoll-1) was without effect whereas 0.75mmoll-1 stimulated transient increases in fluid output. The higher SITS concentration caused no alterations to flow or electrolyte concentrations during maximal stimulation. Carotid plasma [amiloride] (0.05mmoll-1) caused immediate falls in flow rate of 20-30% followed by progressive recovery over 25min to levels above pre-amiloride flow rates despite plasma [amiloride] increasing tenfold. Concurrently, salivary [Na] and [Cl] rose to equal plasma concentrations and [K] fell by 50% indicating blockade of acinar Na/H exchangers and luminal Na channels in the ducts. Increased salivary osmolarity caused the flow recovery. Saliva flow during maximum cholinergic stimulation was reduced by 38-46%. The depression of flow was interpreted as resulting from competition between amiloride and acetylcholine for access to the muscarinic receptors. Plasma [acetazolamide] (0.35-2.5mmoll-1) did not alter saliva outflow during mid-range or maximum flow regimes whereas salivary [Cl] increased and [HCO3] decreased consistent with reduced anion exchange resulting from inhibition of carbonic anhydrase. Combined with bumetanide, acetazolamide (1.5mmoll-1) reduced flow by an additional 18-22% relative to bumetanide alone thereby demonstrating that acinar HCO3 synthesis supported a limited proportion of saliva formation and that some HCO3 secretion was independent of carbonic anhydrase activity.