Prostaglandin generation from gastroduodenal mucosa: Regional and species differences

Ahlquist, David A.; Duenes, Judith A.; Madson, T.H.; Romero, J. Carlos; Dozois, Roger R.; Malagelada, Juan R.

doi:10.1016/0090-6980(82)90183-6

Cited by 58 publications

(12 citation statements)

References 10 publications

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“…Cheung et al (25) also found that during exposure of the canine gastric mucosa to alcohol, aspirin and bile salts, an increase in H+ back-diffusion was accompanied by an increase in GMBF. The processes underlying the elevation of GMBF by topical barrier breakers are speculated to be a response of the mucosal microvasculature to the in creased H+ back-diffusion or to the release of local mediators (18). In the present study, topical application of aspirin resulted in increases of both GMBF and H+ back diffusion.…”

Section: Discussionsupporting

confidence: 47%

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Effect of prostaglandins on mucosal blood flow and aspirin-induced damage in the canine stomach.

Inatomi

Maki

1983

Jpn.J.Pharmacol

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Abstract-This study deals with the action in anesthetized dogs of prostaglandin E2 and F20 given into the celiac artery and the femoral vein on gastric mucosal blood flow and on gastric mucosal damage induced by aspirin. In the non-stimulated stomach , infusion of prostaglandin E2 or F2 into the celiac artery resulted in a marked increase in mucosal blood flow and a sustained decrease, respectively. In contrast, an infusion of pro staglandin E2 into the femoral vein produced a decrease in mucosal blood flow , whereas prostaglandin F21 produced a biphasic response: a transient increase followed by a decrease. It was observed that intravenously infused prostaglandin E2, while reducing mucosal blood flow, significantly diminished mucosal lesions, altered transmucosal potential differences and H+ back-diffusion induced by a topical application of aspirin. The findings indicate that the action of prostaglandins on gastric mucosal blood flow alters depending on the route of administration and that prostaglandins seem to exert gastric cytoprotection through mechanisms other than an increase in mucosal blood flow.

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Section: Discussionsupporting

confidence: 47%

“…infusion, we have concluded that PGE2 and PGF2a exert, respectively, a dilating and a constricting activity on the gastric mucosal vessels. As relatively large amount of PGE2 and PGF2,V are generated in the gastric mucosa (18), both PGs in this tissue probably play an important role in regulating GMBF, at least in dogs.…”

Section: Discussionmentioning

confidence: 99%

Effect of prostaglandins on mucosal blood flow and aspirin-induced damage in the canine stomach.

Inatomi

Maki

1983

Jpn.J.Pharmacol

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“…Also, we found PGE 2 inhibited the spontaneous [Ca 2+ ] i oscillations in cultured ICC. These observations indicate that PGE 2 alters pacemaker currents by activating the ATP-dependent K + channels comprised of K ir 6.2-SUR 2B in ICC and this action of PGE 2 are through EP 2 receptor subtype and also the activation of ATP-dependent K Introduction Prostaglandins (PGs) are widely distributed throughout the gastrointestinal tract and play a significant role in its physiology and pathophysiology [1][2][3]. In particular, PGE 2 is known to contract longitudinal muscle and to relax circular muscle in humans and in various animal species [4,5].…”

Section: Introductionmentioning

confidence: 99%

“…However, this action varies greatly, and depends on PGE 2 concentration, the organ, the species, and even the muscle layer studied [5][6][7]. Previous studies demonstrated that PGE 2 exerts its biological actions through binding to four specific membrane receptor subtypes known as EP 1 , EP 2 , EP 3 and EP 4 [8,9]. These subdividing are the basis of the relative potency of selective agonists and antagonists in both functional and binding studies.…”

Section: Introductionmentioning

confidence: 99%

Activating of ATP-Dependent K+ Channels Comprised of Kir 6.2 and SUR 2B by PGE2 Through EP2 Receptor in Cultured Interstitial Cells of Cajal from Murine Small Intestine

Choi

Yeum

Chang

et al. 2006

Cell Physiol Biochem

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The interstitial cells of Cajal (ICC) are pacemaker cells in gastrointestinal tract and generate an electrical rhythm in gastrointestinal muscles. We investigated the possibility that PGE₂ might affect the electrical properties of cultured ICC by activating ATPdependent K⁺ channels and, the EP receptor subtypes and the subunits of ATP-dependent K⁺ channels involved in these activities were identified. In addition, the regulation of intracellular Ca²⁺ ([Ca²⁺]i) mobilization may be involved the action of PGE₂ on ICC. Treatments of ICC with PGE₂ inhibited electrical pacemaker activities in the same manner as pinacidil, an ATPdependent K⁺ channel opener and PGE₂ had only a dose-dependent effect. Using RT-PCR technique, we found that ATP-dependent K⁺ channels exist in ICC and that these are composed of K_ir 6.2 and SUR 2B subunits. To characterize the specific membrane EP receptor subtypes in ICC, EP receptor agonists and RT-PCR were used: Butaprost (an EP₂ receptor agonist) showed the actions on pacemaker currents in the same manner as PGE₂. However sulprostone (a mixed EP₁ and EP₃ agonist) had no effects. In addition, RT-PCR results indicated the presence of the EP₂ receptor in ICC. To investigate cAMP involvement in the effects of PGE₂ on ICCs, SQ-22536 (an inhibitor of adenylate cyclase) and cAMP assays were used. SQ-22536 did not affect the effect of PGE₂ on pacemaker currents, and PGE₂ did not stimulate cAMP production. Also, we found PGE₂ inhibited the spontaneous [Ca²⁺]i oscillations in cultured ICC. These observations indicate that PGE₂ alters pacemaker currents by activating the ATP-dependent K⁺ channels comprised of K_ir 6.2-SUR 2B in ICC and this action of PGE₂ are through EP₂ receptor subtype and also the activation of ATP-dependent K⁺ channels involves intracellular Ca²⁺ mobilization.

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“…(PGEi) is a major product of arachidonic acid metabolism in gastrointestinal cells [5,6]. They can be quickly synthesized in response to nonspe cific stimuli [7].…”

Section: Introductionmentioning

confidence: 99%

Prostaglandin E2 Modulates Serotonin-and Gastrin/CCK-lmmunoreactive Cells in the Duodenal Mucosa of the Rat

et al. 1997

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Groups of Sprague-Dawley rats were given placebo or prostaglandin E₂ (PGE₂) at 25 or 5,000 μg/kg or 15, R,15-methyl-PGE₂ (MePGE₂) at 5 or 50 μg/ kg, twice daily, orally, for 1 month. Histological sections from the proximal duodenum were processed for immunohistochemistry and the volume density of immunoreactive endocrine cells was determined using point-counting grids. The surface density of the villous lining was estimated by using a cycloid test system. Thereafter, the total volumes of endocrine cells and the total surface area of the villous lining were calculated after estimating the mucosal volume. The volume density of serotonin-immunoreactive cells was increased in the duodenum of rats given 25 or 5,000 μg/kg PGE₂ (p < 0.05). The total volume of these cells increased in the animals given 25 μg/kg PGE₂ (p < 0.05). The total volume of gastrin/CCK-immunoreactive cells was higher in rats given 25 μg/kg PGE₂ or 50 μg/kg MePGE₂ than in controls (p < 0.05). The volume density of somatostatin-immunoreactive cells increased in rats given 5 μg/kg MePGE₂, but the total volumes were not different between the groups. The area of somatostatin-immunoreactive cell profiles was enlarged in the animals given 5,000 μg/kg PGE₂ (p < 0.05). The mucosal volume was enlarged by prostaglandins. The epithelial thickness increased in rats given the highest doses of PGE₂ (p < 0.05). The concentration of motilin-like immunoreactivity increased in the duodenum of rats given 5 μg/kg MePGE₂ (p < 0.05). We conclude that oral administration of PGE₂ for 1 month increased the total volumes of serotonin- and gastrin-CCK-immunoreactive cells and the tissue concentration of motilin-like immunoreactivity, which indicates that prostaglandins modulate endocrine cells in a stable steady-state condition.

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Prostaglandin generation from gastroduodenal mucosa: Regional and species differences

Cited by 58 publications

References 10 publications

Effect of prostaglandins on mucosal blood flow and aspirin-induced damage in the canine stomach.

Effect of prostaglandins on mucosal blood flow and aspirin-induced damage in the canine stomach.

Activating of ATP-Dependent K<sup>+</sup> Channels Comprised of K<sub>ir</sub> 6.2 and SUR 2B by PGE<sub>2</sub> Through EP<sub>2</sub> Receptor in Cultured Interstitial Cells of Cajal from Murine Small Intestine

Prostaglandin E<sub>2</sub> Modulates Serotonin-and Gastrin/CCK-lmmunoreactive Cells in the Duodenal Mucosa of the Rat

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