Stimulation of Cl/HCO3 exchange in rat duodenal brush border membrane vesicles by cAMP.

Brush border membrane vesicles have been used to study the regulation of rat duodenal HCO3 secretion. When vesicles were loaded with cAMP and ATP SITS-sensitive Cl/HCO3 exchange (unidirectional 36Cl influx in response to an outward-facing OH/HCO3 gradient) was stimulated by approximately 25%. In contrast, there was no effect of cAMP upon SITS-insensitive 36Cl uptake. The stimulation of Cl/HCO3 exchange caused by cAMP was abolished in the presence of a specific heat-stable cAMP-dependent protein kinase inhibitor. These results suggest that Cl/HCO3 exchange, and hence HCO3 secretion, is regulated by cAMP via phosphorylation of some component of the membrane associated with the transport protein.