Central and Peripheral Effects of Prostaglandin E2 and Enprostil on Exocrine Pancreatic Secretion in Rats

Sautereau, Denis; Chovet, M.; Chariot, J; Tsocas, Annick; Rozé, C

doi:10.1097/00006676-198904000-00010

Cited by 5 publications

(2 citation statements)

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“…Furthermore, the PGE 1 analog tested (alprostadil) inhibited salivation induced by NA or MC, confirming previous results (22). These results are in agreement with others that showed an inhibitory effect of PGs on exocrine pancreatic secretion (16). There is a similar response of mesenteric vessels to LPS to those of the SMG (VE Mendizabal, A Lomniczi, C Mohn, V Rettori, and E Adler-Graschinsky, unpublished data).…”

Section: Discussionsupporting

confidence: 90%

Inhibition of salivary secretion by lipopolysaccharide: possible role of prostaglandins

Lomniczi

Mohn

Faletti

et al. 2001

American Journal of Physiology-Endocrinology and Metabolism

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Inducible (calcium-independent) nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are important in the regulation of the function of different organs during infection. A single dose of lipopolysaccharide (LPS; 5 mg/kg ip) within 6 h increased NOS activity (20%) and prostaglandin E (PGE) content (100%) in submandibular glands (SMG) and blocked stimulated salivary secretion in adult male rats. The administration of an iNOS synthesis inhibitor, aminoguanidine (AG), with LPS decreased NOS activity and PGE content. Furthermore, the administration of meloxicam (MLX), an inhibitor of COX-2, blocked the increase in PGE and the production of NO. The incubation of slices of SMG in the presence of 3-morpholinosydnonimine, a donor of NO, increased the release of PGE highly significantly. The incubation of SMG in the presence of a PGE(1) analog (alprostadil) increased the production of NO. These results indicate that LPS activates NOS, leading to NO release, which activates COX, generating PGEs that act back to further activate NOS, causing further generation of PGEs by activation of COX. Because the alprostadil administration inhibited stimulated salivation, LPS-induced inhibition of salivation appears to be caused by increased PGE production. Diminished salivary secretion produces poor oral health; thus the use of COX-2 inhibitors to counteract the effects of inhibited salivation should be considered.

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Section: Discussionsupporting

confidence: 90%

Inhibition of salivary secretion by lipopolysaccharide: possible role of prostaglandins

Lomniczi

Mohn

Faletti

et al. 2001

American Journal of Physiology-Endocrinology and Metabolism

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“…In the normal pancreas, exogenously applied PGE 2 has an inhibitory effect on CCK-stimulated amylase secretion of the rat pancreas, both in vitro [19] and in vivo [5,24]. PGE 2 directly inhibits the enzyme secretion induced by both Ca 2+ -and cAMP-mediated secretagogues [19], indicating complex effects on intracellular signalling pathways.…”

Section: Introductionmentioning

confidence: 99%

Inhibitory effects of PGE 2 on K + currents and Ca 2+ oscillations in rat pancreatic acinar cells

Lee

Kim

Choi

et al. 2002

Pfl�gers Archiv European Journal of Physiology

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Prostaglandin E(2) (PGE(2)) inhibits pancreatic enzyme secretion and shows a protective action against pancreatitis. In this study, we tested the effects of PGE(2) on the slowly activating voltage-dependent K(+) channel current ( I(Ks)) and cholecystokinin (CCK)-induced oscillations of cytosolic [Ca(2+)] ([Ca(2+)](i)) in rat pancreatic acini (RPA). I(Ks) in RPA is reportedly augmented by both Ca(2+)- and cAMP-mediated secretagogues. PGE(2) (10(-7) M) decreased the amplitude of I(Ks), an effect that was more prominent following prior stimulation with secretin. The application of the membrane-permeable cAMP analogue 8-Br-cAMP prevented the effect of PGE(2) on I(Ks). The Ca(2+)-mediated augmentation of I(Ks) by ACh was unaffected by pretreatment with PGE(2). Using fura-2 fluorescence ratiometry to assess [Ca(2+)](i), CCK (

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Central and peripheral effects of prostaglandin E2 and enprostil on gastric acid secretion in the rat

Sautereau

Chicau-Chovet

Tsocas

et al. 1991

European Journal of Pharmacology

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Central and Peripheral Effects of Prostaglandin E2 and Enprostil on Exocrine Pancreatic Secretion in Rats

Cited by 5 publications

References 0 publications

Inhibition of salivary secretion by lipopolysaccharide: possible role of prostaglandins

Inhibition of salivary secretion by lipopolysaccharide: possible role of prostaglandins

Inhibitory effects of PGE 2 on K + currents and Ca 2+ oscillations in rat pancreatic acinar cells

Central and peripheral effects of prostaglandin E2 and enprostil on gastric acid secretion in the rat

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