1. In pentobarbitone-anaesthetized dogs with constant-flow vascular perfusion of nasal mucosa on both sides, nasal airway resistance, vascular resistance, vascular capacitance (via changes in total venous outflow) and blood flow in the anterior and posterior venous systems were measured. 2. Electrical stimulation of the cut peripheral ends of the cervical sympathetic trunk, caudal nasal nerve, or major palatine nerve increased vascular resistance and decreased vascular capacitance and airway resistance. Propranolol and atropine had no effect on the responses while bretylium completely abolished them; phentolamine greatly lessened the vascular resistance response and partially decreased the vascular capacitance and airway responses. Hence, sympathetic stimulation causes constriction of the resistance vessels via alpha-adrenergic mechanism and constriction of capacitance vessels via alpha-adrenergic as well as some non-adrenergic and non-cholinergic mechanisms. 3. Denervation of the cervical sympathetic trunk, caudal nasal nerve and major palatine nerve decreased nasal vascular resistance and increased vascular capacitance and airway resistance, suggesting tonic sympathetic discharge to nasal mucosa via caudal nasal and major palatine nerves. 4. Electrical stimulation of the nerve of pterygoid canal decreased vascular resistance but increased vascular capacitance (in the posterior venous system) and airway resistance to low-voltage stimulation (below 10 V), and decreased vascular capacitance (in the anterior venous system) and airway resistance to high-voltage stimulation (above 10 V). Hexamethonium reversed the vascular resistance response as well as vascular capacitance and airway responses to high-voltage stimulation. Bretylium and phentolamine enhanced the vascular resistance response and reversed vascular capacitance and airway resistance responses to high-voltage stimulation. Hence, low-voltage stimulation results in parasympathetic dilatation of resistance and capacitance vessels whereas high-voltage stimulation results in parasympathetic dilatation of resistance vessels and sympathetic constriction of capacitance vessels. The parasympathetic vasodilatation was atropine resistance and the sympathetic vasoconstriction was partially via alpha-adrenergic mechanisms. 5. Denervation of the nerve of pterygoid canal did not affect vascular resistance, vascular capacitance or airway resistance suggesting negligible tonic parasympathetic and sympathetic discharges to nasal blood vessels via the nerve. 6. Simultaneous optimal stimulation of sympathetic and parasympathetic nerves resulted in vasoconstriction, especially in capacitance vessels, suggesting sympathetic predominance over parasympathetic control.