%0 Journal Article %1 Puurunen1987 %A Puurunen, J. %A Lohse, M. J. %A Schwabe, U. %D 1987 %J Naunyn Schmiedebergs Arch Pharmacol %K & AMP/antagonists Activation/drug Animals Bucladesine/pharmacology C/metabolism Carbachol/pharmacology Cimetidine/pharmacology Cyclic Dibutyryl Enzyme Esters/pharmacology Forskolin/pharmacology GMP/pharmacology Gastric/metabolism Histamine/pharmacology Inhibitors/pharmacology Inositol Kinase Male Parietal Phorbol Phosphates/*metabolism Phosphates/antagonists Phosphodiesterase Protein Pyrrolidinones/pharmacology Rats Rolipram Strains Sugar effects inhibitors/*metabolism inhibitors/*physiology Cell Mice %N 5 %P 471-7 %T Interactions between intracellular cyclic AMP and agonist-induced inositol phospholipid breakdown in isolated gastric mucosal cells of the rat %U http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2830543 %V 336 %X The interactions between putative second effector mechanisms for hydrogen ion secretion were studied in isolated gastric cell preparations of the rat containing 60-70% parietal cells. Dibutyryl-cAMP and the compounds which increased the level of cAMP (histamine plus rolipram and forskolin plus rolipram) inhibited the carbachol-induced accumulation of 3Hinositol tris-, bis- and monophosphate. There was both a temporal and quantitative correlation between the increase in cAMP and the inhibition of the accumulation of 3Hinositol phosphates. Cimetidine attenuated the inhibitory effect of histamine on the formation of 3Hinositol phosphates. The enhancement of the accumulation of 3Hinositol phosphates by various concentrations of carbachol affected neither the basal nor the histamine-stimulated cAMP levels. In contrast to dibutyryl-cAMP, dibutyryl-cGMP did not modify the carbachol-induced formation of 3Hinositol phosphates. The biologically active phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), which activates protein kinase C, inhibited both the basal and carbachol-induced accumulation of 3Hinositol phosphates. We suggest that the inhibition of the formation of inositol trisphosphate by the increase in the intracellular level of cAMP and by the activation of protein kinase C might be intracellular negative feedback systems which prevent the overreaction of the acid-secreting parietal cells under the simultaneous influence of the physiological gastric secretagogues.

@article{Puurunen1987, abstract = {The interactions between putative second effector mechanisms for hydrogen ion secretion were studied in isolated gastric cell preparations of the rat containing 60-70% parietal cells. Dibutyryl-cAMP and the compounds which increased the level of cAMP (histamine plus rolipram and forskolin plus rolipram) inhibited the carbachol-induced accumulation of [3H]inositol tris-, bis- and monophosphate. There was both a temporal and quantitative correlation between the increase in cAMP and the inhibition of the accumulation of [3H]inositol phosphates. Cimetidine attenuated the inhibitory effect of histamine on the formation of [3H]inositol phosphates. The enhancement of the accumulation of [3H]inositol phosphates by various concentrations of carbachol affected neither the basal nor the histamine-stimulated cAMP levels. In contrast to dibutyryl-cAMP, dibutyryl-cGMP did not modify the carbachol-induced formation of [3H]inositol phosphates. The biologically active phorbol ester, 12-O-tetradecanoylphorbol-13-acetate (TPA), which activates protein kinase C, inhibited both the basal and carbachol-induced accumulation of [3H]inositol phosphates. We suggest that the inhibition of the formation of inositol trisphosphate by the increase in the intracellular level of cAMP and by the activation of protein kinase C might be intracellular negative feedback systems which prevent the overreaction of the acid-secreting parietal cells under the simultaneous influence of the physiological gastric secretagogues.}, added-at = {2010-12-14T18:12:02.000+0100}, author = {Puurunen, J. and Lohse, M. J. and Schwabe, U.}, biburl = {https://www.bibsonomy.org/bibtex/2d43e70771d6917c859827546d09840ed/pharmawuerz}, endnotereftype = {Journal Article}, interhash = {e5478516017cc125a747d3a09828e12f}, intrahash = {d43e70771d6917c859827546d09840ed}, issn = {0028-1298 (Print) 0028-1298 (Linking)}, journal = {Naunyn Schmiedebergs Arch Pharmacol}, keywords = {& AMP/antagonists Activation/drug Animals Bucladesine/pharmacology C/metabolism Carbachol/pharmacology Cimetidine/pharmacology Cyclic Dibutyryl Enzyme Esters/pharmacology Forskolin/pharmacology GMP/pharmacology Gastric/metabolism Histamine/pharmacology Inhibitors/pharmacology Inositol Kinase Male Parietal Phorbol Phosphates/*metabolism Phosphates/antagonists Phosphodiesterase Protein Pyrrolidinones/pharmacology Rats Rolipram Strains Sugar effects inhibitors/*metabolism inhibitors/*physiology Cell Mice}, month = Nov, note = {Puurunen, J Lohse, M J Schwabe, U In Vitro Research Support, Non-U.S. Gov't Germany, west Naunyn-Schmiedeberg's archives of pharmacology Naunyn Schmiedebergs Arch Pharmacol. 1987 Nov;336(5):471-7.}, number = 5, pages = {471-7}, shorttitle = {Interactions between intracellular cyclic AMP and agonist-induced inositol phospholipid breakdown in isolated gastric mucosal cells of the rat}, timestamp = {2010-12-14T18:22:56.000+0100}, title = {Interactions between intracellular cyclic AMP and agonist-induced inositol phospholipid breakdown in isolated gastric mucosal cells of the rat}, url = {http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=2830543}, volume = 336, year = 1987 }