(-32.0,uequiv H+ kg-' 15 min-'). This is followed by a slow phase of tachyphylaxis (-9-4 ,equiv H+ kg-' 15 min-') up to 5 hr of stimulation.

No abstract

Bromocriptine administered both orally and intravenously potentiated gastric acid secretion in response to submaximal pentagastrin stimulation in cats. Bromocriptine did not increase the maximum acid secretion in response to pentastrin, not did it stimulate basal acid secretion. Potentiation was observed in normal and vagotomized animals which precludes involvement of the vagi in the response. The mechanism of action of this compound on the stomach does not appear to be mediated through stimulation of dopaminergic receptors as no potentiation was observed with dopamine infusions. It is argued that the bromocriptine potentiation of gastric acid secretion may be a demonstration of 5-hydroxytryptamine or alpha-adrenergic antagonism. However, the potentiation observed with daily oral bromocriptine treatment had disappeared by the eighth day and may correlate with the disappearance of gastric side effects noted in patients on bromocriptine treatment.