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Abstract
Background: To ascertain the mechanism for rebound acid hypersecretion after treatment with an H2-receptor blocker, we investigated the effects of ranitidine on gastric H+, K+-adenosine triphosphatase (ATPase) in rats, Methods: Male Wistar rats received ranitidine (1-50mg/kg body weight intraperito-neally twice a day for 5 days). The rats were starved for 15 h after the last treatment and then killed, and gastric vesicles containing H+, K+-ATPase were prepared. Results: Treatment with ranitidine dose-dependently increased protein content in the gastric vesicular fraction purified from the gastric mucosa without changing total protein content. Ranitidine also increased the content of a 94,000-dalton protein, the catalytic subunit of H+, K+-ATPase. On the other hand, ranitidine did not affect the specific activity of the enzyme (μmol/min/mg of the gastric vesicular protein). Since gastric vesicles in the fasting state mainly consist of the tubulovesicular membrane, these results suggest that ranitidine administration increases total tubulovesicular H+, K+-ATPase content (μmol/min/rat) by increasing the number of tubulovesicles per parietal cell. The ranitidine-induced increase in total tubulovesicular H+, K+-ATPase activity was still evident 1 week after treatment and returned to control level 1 month later. Conclusions: All these findings suggest that the increased content and total activity of tubulovesicular H+, K+-ATPase after ranitidine treatment may contribute to the mechanism for acid rebound after H2-blocker therapy.