Gastroduodenal HCO3-secretion in anesthetized rats: effects of 16,16-dimethyl PGE2, topical acid and acetazolamide.

Alkaline secretion was measured in the whole stomach and in the proximal duodenum (2 cm proximal to the outlet of the common bile duct) of anesthetized rats, under basal conditions and in response to topical acid and 16,16-dimethyl PGE2 (16-dmPGE2) given by various routes. Gastric alkaline secretion was unmasked by intraduodenal administration of omeprazole (30 mg/kg). Both the stomach and duodenum consistently secreted bicarbonate in amounts of 0.2-0.4 microEq/15 min and 1.5-2 microEq/15 min as a basal secretion, respectively. 16-dmPGE2, either given subcutaneously (1-30 micrograms/kg), intravenously (3 micrograms/kg/hr) or by topical application for 30 min (0.3-10 micrograms/ml), (concentration)-dependently increased HCO3- secretion in both tissues, but this effect disappeared quickly after sacrifice with KCI (i.v.). Stimulation of HCO3- secretion was also caused by topical acid to the stomach (100 mM HCI for 10 min) or to the duodenum (10 mM HCI for 10 min), but was completely blocked by pretreatment with indomethacin (5 mg/kg, s.c.). Acetazolamide, given subcutaneously at 100 mg/kg, which gives over 80% inhibition of carbonic anhydrase activity in the gastroduodenal mucosa, had no effect on either basal or stimulated HCO3- secretion caused by 16-dmPGE2 (10 micrograms/kg, s.c.). These results indicate that both endogenous and exogenous (16-dmPGE2) prostaglandins stimulate alkaline secretion in the gastroduodenal mucosa of rats, and this mechanism is independent from the carbonic anhydrase activity of the tissue.