HCO3- secretion in rat duodenum after treatment with omeprazole and ranitidine.
The bicarbonate secretion by the duodenal mucosa, which is stimulated by luminal acid, is very probably important in mucosal protection against the acid. It was of interest to investigate whether long-term deprivation of the mucosa of this acid stimulus affected the alkali secretion. Sprague-Dawley rats were treated for 4-6 weeks with either omeprazole, 14 mg/kg body weight twice daily, or ranitidine, 300 mg/kg twice daily, by means of gastric intubation. The rate of bicarbonate secretion by the duodenal mucosa was determined in situ by continuous titration. Neither the basal secretion nor the increase in secretion in response to stimulation by prostaglandin E2 or luminal acid (pH 2.0 for 5 or 60 min) differed in treated animals from that in controls that had received placebo (p greater than 0.05). Thus, 4-6 weeks of treatment with omeprazole or ranitidine did not reduce duodenal mucosal bicarbonate secretion in the rat, nor did these drugs diminish the ability of this mucosa to respond to prolonged luminal acidification or luminally administered prostaglandin E2.
Knutson
L
L
Flemström
G
G
Gustavsson
S
S
Jedstedt
G
G
Lönnerholm
G
G
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D015232:Dinoprostone; D004386:Duodenum / Q000187:drug effects*; D007413:Intestinal Mucosa / Q000187:drug effects; D007419:Intestinal Secretions / Q000187:drug effects*; D008297:Male; D009853:Omeprazole / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology; D011899:Ranitidine / Q000494:pharmacology*; D051381:Rats; D011919:Rats, Inbred Strains
D001639:Bicarbonates; D011458:Prostaglandins E; D011899:Ranitidine; D015232:Dinoprostone; D009853:Omeprazole