Effect of prostaglandin E2 (PGE2) on mucus secretion by mucocytes of the fundal part of the rat stomach has been studied electron microscopically, morphometrically and biochemically. PGE2 is found to stimulate synthesis of glycoproteins and their secretion by the mucocytes that results in increasing the relative volume of Golgi complex and in decreasing that of secretory granules. Actinomycin does not affect and cycloheximide blocks the stimulating activity of prostaglandin.
View Article and Find Full Text PDFBoth prostaglandin E2 (PGE2) and histamine activated the adenylate cyclase system of rat gastric cells. Parietal acid-producing cells of the stomach were the target-cells for histamine, while PGE2 affected the mucous cells of gastric glands. The stimulating effect of PGE2 on mucus production occurred due to activation of protein synthesis.
View Article and Find Full Text PDFPentagastrin as well as transmitters of its effect histamine and cAMP, affecting the HCl secretion, increased the gastric mucus secretion apparently due to stimulation of HCl production. This assumption is supported by experiments in which the histamine effect was not inhibited by cycloheximide but was completely eliminated in presence of burimamide--a drug blocking histamine H2-receptors. Prostaglandin E2 which inhibited distinctly basal secretion of HCl but did not affect the pepsin secretion, elevated markedly the mucus production.
View Article and Find Full Text PDFIsolated cells of rat gastric mucosa were obtained by treatment of rat stomach with pronase. Two fractions were isolated, one of which was rich (up to 90%) and the second one poor (to 25%) of parietal cells. Using specific antagonists and agonists of H1- and H2-receptors of histamine (diphenhydramine, metiamide, cimetidine, impromidine, dimaprit) the H2-receptors of histamine were shown to be localized in parietal cells.
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