The effect of Ostertagia circumcincta on the secretory function of the ovine abomasum was studied in vivo and in vitro. In vivo, sheep were infected with larval or adult parasites and the changes in serum pepsinogen, serum gastrin and abomasal pH monitored. In vitro, the effect of worm extracts and incubates on the secretion of gastrin, somatostatin and pepsinogen were investigated using segments or dispersed cells of ovine abomasal mucosa. Using these, and a further perifusion technique, the pharmacology of gastrin and somatostatin secretion in the sheep was also investigated. The in vivo study revealed that adult worms transferred directly into the abomasum of parasite-naive sheep initiate immediate changes in serum pepsinogen, gastrin and abomasal pH, showing that larval stages are not essential for the pathophysiological changes. These changes also occurred following infection with larvae but not until about five days post-infection. The increase in abomasal pH and serum gastrin occurred at a similar time, regardless of the dose of larvae or the route of administration. Serum pepsinogen levels increased before gastrin and pH. The normal range for serum pepsinogen, serum gastrin and abomasal pH in the parasite-free sheep were defined (0-500 U tyrosine/litre, 12-64 pM and 2.34-3.26 respectively). When abomasal pH rose and was maintained above pH 5.5 in sheep infected with larvae, serum gastrin levels rapidly returned to normal. When pH subsequently declined below 5.5, gastrin rapidly returned to elevated levels. By three weeks after infection of parasite-naive sheep with larvae, pH had returned to the normal range despite the continued elevation of serum gastrin. Infection with adults and larvae significantly increased the wet weight of the abomasum and this occurred within 8 days of infection with adult worms. Tissue gastrin levels were decreased by infection. In vitro, solutions prepared with larvae and adult O. circumcincta had no effect on, or inhibited, gastrin release. These same solutions had no effect on, or stimulated, somatostatin secretion. Inhibition of gastrin secretion was always accompanied by increased somatostatin secretion although the converse was not true. Worm-derived solutions that inhibited gastrin release were possibly contaminated by microorganisms. Incubation of medium contaminated by an inoculum of abomasal content but without worms produced solutions that potently stimulated somatostatin and inhibited gastrin release. The pharmacological study revealed that mechanisms that have been identified in the regulation of gastrin secretion in other animals are present in the sheep. GRP, nicotine and carbachol but not adrenaline stimulated gastrin secretion from segments of antral mucosa in a concentration-dependent manner. Carbachol did not consistently inhibit somatostatin secretion and in most experiments somatostatin and carbachol release were both stimulated. Atropine inhibited basal gastrin release from segments of mucosa indicating a degree of tonic cholinergic discharge. Atropine partially or completely prevented the gastrin response to carbachol. VIP and GIP both stimulated somatostatin secretion but had no effect on gastrin, suggesting that somatostatin either does not restrain gastrin in the sheep or that this is maximal at basal levels. Somatostatin antiserum was not associated with increased gastrin secretion in most experiments.