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Omeprazole, a proton pump inhibitor, exerts its effects by binding covalently to the H+/K+-ATPase that is located in the apical membrane of gastric parietal cells. However, its effects on pepsinogen-producing cells have not been investigated in detail and results of previous relevant studies on pepsinogen secretion are conflicting. Gastric mucosal cells proliferate and differentiate under an acidic environment in the gastric lumen. Thus, it is probable that omeprazole-induced reduced acidity in the gastric lumen has some influences on the proliferation and differentiation of the mucosal cells. As the first step to elucidate the effects of omeprazole on pepsinogen-producing cells, we analyzed the processes from the gene expression to the secretion of pepsinogen in vivo in adult rat glandular stomach. Next, we investigated the effects of omeprazole on the development of rat gastric mucosa biochemically and histologically, with special reference to pepsinogen expression as a marker of terminal differentiation.

Scanning electron microscopy (SEM) of corrosion casts allows a clearer three-dimensional view of fine vascular architecture than conventional light or transmission electron microscopy of sectioned or injected tissue specimens (1–8). Positional relations of each vessel to the tissue elements cannot be examined in the cast samples, since the cast itself is observed in isolation from the surrounding tissues. However, SEM of vascular corrosion casts has already shown itself to be valuable and useful in the study of microvascular architecture in various organs and tissues, including the gastrointestinal canal (9–24).