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Beubler, E; Hinterleitner, T; Horina, G.
Protein kinase C and intestinal fluid secretion: involvement of prostaglandin E2 but not of 5-hydroxytryptamine.
Eur J Pharmacol. 1990; 182(3):543-548 Doi: 10.1016/0014-2999(90)90053-9
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Leading authors Med Uni Graz
Beubler Eckhard
Co-authors Med Uni Graz
Hinterleitner Thomas
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Abstract:
To determine the role of protein kinase C in the regulation of intestinal fluid transport, experiments were performed with the rat jejunum in vivo, using the active phorbol ester, 4-beta-phorbol 12-myristate 13-acetate (PMA), as stimulator of protein kinase C. Intraluminally administered PMA dose dependently reversed the net fluid absorption to net fluid secretion and significantly increased prostaglandin E2 (PGE2) but not 5-hydroxytryptamine (5-HT) output into the lumen. Mucosal cyclic AMP levels remained unchanged by PMA. Indomethacin inhibited the increase in PGE2 output and partially reduced the secretory response to PMA. Ketanserin was without effect whereas verapamil totally blocked the secretory response to PMA. It is concluded that intestinal fluid secretion, stimulated by activation of protein kinase C is partly mediated by PGE2 release. PGE2 may facilitate calcium entry rather than increase intracellular calcium through activation of cyclic AMP. Protein kinase C appears to play an important role as an intermediate in phosphoinositol hydrolysis, which is initiated by 5-HT, and finally induces fluid secretion via PGE2.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Body Fluids - secretion
Cyclic AMP - biosynthesis
Dinoprostone - physiology
Dose-Response Relationship, Drug - physiology
Female - physiology
Indomethacin - pharmacology
Intestinal Mucosa - drug effects
Jejunum - drug effects
Ketanserin - pharmacology
Protein Kinase C - metabolism
Rats - metabolism
Rats, Inbred Strains - metabolism
Serotonin - physiology
Tetradecanoylphorbol Acetate - pharmacology
Verapamil - pharmacology

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