1. The effects of electrical vagal stimulation on frequency-dependent gastric acid secretion were investigated in urethane-anaesthetized rats in vivo. 2. Stimulation at 4, 16 or 32 Hz was performed in rats treated with atropine (1 mg kg-1, i.v.), hexamethonium (10 mg kg-1, i.v. bolus and 1 mg kg-1 min-1, i.v. infusion) or atropine and hexamethonium (doses as above); in some experiments pentagastrin (1.2 micrograms kg-1 h-1, i.v. infusion) was infused prior to stimulation. 3. Maximal acid secretion occurred at 16 Hz. This was significantly reduced but not abolished by atropine or hexamethonium and completely abolished after atropine and hexamethonium. In the presence of pentagastrin, the acid secretory response to 16 Hz stimulation was augmented, atropine or hexamethonium reduced stimulated secretion by about 70%, whereas atropine and hexamethonium completely abolished stimulated secretion. 4. In rats in which the vagus nerve was pretreated with capsaicin 10-14 days before experimentation there was a significant reduction (by about 40%) in stimulated acid secretion at 16 Hz, which was virtually abolished by atropine treatment. After acute treatment of the vagus nerve with capsaicin (at the time of experimentation) maximally stimulated acid secretion was significantly reduced by about 50%. 5. Taken together, these results indicate that capsaicin-sensitive afferent fibres contribute to the acid secretory response induced by electrical vagal stimulation in the rat. Based on pharmacological evidence, the capsaicin-sensitive afferent fibres may be cholinergic, since atropine and hexamethonium totally abolish vagal stimulation-induced acid secretion.