Pepsin secretion in the anaesthetized cat and the effect of sympathetic nerve stimulation.

1. Experiments were performed on chloralose anaesthetized cats and gastric mucosal blood flow, acid and pepsin secretions were measured. Gastric mucosal pepsin and protein contents were measured at the end of the experiments which were done in three groups: gastrin (A), vagal (B), vagal and sympathetic nerve (C) stimulations. 2. Vagal stimulation significantly reduced (76%) the pepsin content of gastric mucosa compared with gastrin stimulated animals, none of which secreted pepsin. 3. The sum of the secreted and extracted pepsins for all the three groups was not significantly different. There was no significant difference in the extracted protein from any of the groups. 4. Gastric mucosal blood flow, acid and pepsin outputs all had significant correlations with time during the first 70 min of vagal stimulation. During the period 80-160 min of vagal stimulation acid secretion and mucosal blood flow were not correlated with time but pepsin output declined significantly. From 170 to 220 min of vagal stimulation, acid and pepsin outputs and mucosal blood flow were not correlated with time. 5. The assumed pepsin store during each period was calculated and after 40 min of vagal stimulation there is a constant percentage pepsin output from this assumed store. 6. There is some data to suggest that pepsinogen synthesis was occurring during the period 170-220 min of vagal stimulation. 7. Sympathetic nerve stimulation which started at 160 min after the beginning of sustained vagal stimulation, significantly inhibited gastric acid secretion and mucosal blood flow, and in addition it significantly inhibited pepsin secretion. This is consistent with the hypothesis that sympathetic nerve inhibition of gastric mucosal function is mediated by a vasoconstrictor mechanism.