1. In the urethane-anaesthetized ferret vagotomy (cervical and abdominal) and hexamethonium both produced an increase in gastric corpus pressure after treatment with atropine and guanethidine, section of the greater splanchnic nerves and adrenalectomy. 2. The pressure increase was due to an interruption of a tonic vagal drive to the intramural non-adrenergic, non-cholinergic inhibitory neurones. 3. The GABAB receptor agonist baclofen (8 mg/kg s.c.) produced an increase in gastric pressure and enhanced the amplitude of the rhythmic contractions. Baclofen was without effect in vagotomized animals. 4. In the presence of atropine, guanethidine, adrenalectomy and section of the greater splanchnic nerves, baclofen produced only a slight enhancement of rhythmic contractions but the large increase in gastric pressure was still present. Under the above conditions the effects of baclofen on the whole stomach were virtually identical to those observed in the corpus region alone. 5. Baclofen was without effect on the magnitude of the corpus relaxation produced by the submaximal vagal efferent stimulation in the presence of atropine. 6. These results demonstrate that the GABAB agonist baclofen, probably acting at a central site, enhanced rhythmic gastric activity by increasing the vagal drive to the intramural cholinergic neurones. Simultaneously gastric pressure was increased primarily by a reduction in the tonic vagal drive to the intramural non-adrenergic, non-cholinergic inhibitory neurones in the corpus region. The results of both the baclofen and vagotomy studies further demonstrate the importance of the vagal innervation of the non-adrenergic, non-cholinergic inhibitory neurones in the regulation of gastric pressure.