Phosphodiesterase isozymes involved in regulation of HCO3− secretion in isolated mouse duodenum in vitro

Hayashi, M; Kita, Kazutomo; Ohashi, Yumi; Aihara, Eitaro; Takeuchi, Koji

doi:10.1016/j.bcp.2007.07.029

Cited by 12 publications

(11 citation statements)

References 20 publications

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“…In general, the fundamental properties of PDE isozymes are well preserved among species. We recently demonstrated in isolated mouse duodenum in vitro that the response of HCO 3 Ϫ to PGE 2 is regulated by both PDE1 and PDE3, whereas the response to NO is modulated by only PDE1 (Hayashi et al, 2007). We also examined in this study the gene expression of PDE isozymes (PDE1ϳPDE5), including their splicing variants, in the mouse stomach, and we confirmed that they all clearly expressed in this tissue.…”

Section: Discussionsupporting

confidence: 65%

“…Thus, there is no doubt that cGMP, but not cAMP, plays a role in the local regulation of gastric HCO 3 Ϫ secretion. We previously reported that IBMX, a nonselective PDE inhibitor, markedly increased duodenal HCO 3 Ϫ secretion induced by not only PGE 2 but also NOR-3 (Takeuchi et al, 1997b;Hayashi et al, 2007). Likewise, the duodenal response to PGE 2 was also enhanced by vinpocetine, the PDE1 inhibitor, and cilostamide, the PDE3 inhibitor, whereas the response to NOR-3 was potentiated only by vinpocetine (Hayashi et al, 2007).…”

Section: Discussionmentioning

confidence: 92%

“…The stomach was opened along the greater curvature and stripped off the muscular layers under a microscope (SZ-PT; Olympus, Tokyo, Japan). The tissues (the corpus mucosa) were then mounted between two halves of a lucite chamber, the exposed area being 12.5 mm 2 , and they were bathed in unbuffered saline (154 mM Na ϩ and 154 mM Cl Ϫ ) gassed with 100% O 2 on the mucosal side and HCO 3 Ϫ Ringer's solution (140 mM Na ϩ , 120 mM Cl Ϫ , 5.4 mM K ϩ , 1.2 mM Mg 2ϩ , 1.2 mM Ca 2ϩ , 1.4 mM HPO 4 2Ϫ , 2.4 mM H2PO 4 Ϫ , 25 mM HCO 3 Ϫ , 10 mM glucose, and 0.001 mM indomethacin) gassed with 95% O 2 , 5% CO 2 on the serosal side (Seidler et al, 1997;Tuo et al, 2006;Hayashi et al, 2007). These solutions were warmed at 37°C and continuously circulated by a gas-lift system.…”

Section: Methodsmentioning

confidence: 99%

“…To disclose the profiles of the subtype-selective PDE inhibitors would be helpful for eliminating the adverse influences of these agents in the body, including the gastrointestinal tract. We recently reported using the isolated mouse duodenum in vitro that the response of HCO 3 Ϫ to PGE 2 is regulated by both PDE1 and PDE3, whereas the response to NO is modulated by only PDE1 (Hayashi et al, 2007). It remains, however, unexplored which PDE isozyme(s) is involved in the regulation of gastric HCO 3 Ϫ secretion.…”

Section: The Secretion Of Hcomentioning

confidence: 99%

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Phosphodiesterase Isozymes Involved in Regulation of Secretion in Isolated Mouse Stomach in Vitro

Kita

Takahashi²,

Ohashi³

et al. 2008

J Pharmacol Exp Ther

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(Ϯ)-(E)-4-Ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamide](NOR-3), a nitric-oxide (NO) donor, is known to increase HCO 3 Ϫ secretion in rat stomachs, intracellularly mediated by cGMP; yet, there is no information about the phosphodiesterase (PDE) isozyme involved in this process. We examined the effects of various isozyme-selective PDE inhibitors on the secretion of HCO 3 Ϫ in the mouse stomach in vitro and the type(s) of PDE isozymes involved in the response to NO. The gastric mucosa of DDY mice was stripped of the muscle layer and mounted on an Ussing chamber. HCO 3 Ϫ secretion was measured at pH 7.0 using a pH-stat method and by adding 2 mM HCl. NOR-3, 8-bromoguanosine 3Ј,5Ј-cyclic monophosphate (8-Br-cGMP), and various PDE inhibitors were added to the serosal side. Vinpocetine (PDE1 inhibitor) or zaprinast (PDE5 inhibitor) was also added serosally 30 min before NOR-3 or 8-Br-cGMP. Both NOR-3 and 8-Br-cGMP stimulated HCO 3 Ϫ secretion in a dosedependent manner, and the response to NOR-3 was significantly inhibited by methylene blue. Likewise, the secretion induced by NOR-3 or 8-Br-cGMP was significantly attenuated by 6-((2S,3S)-3-(4-chloro-2-methylphenylsulfonylaminomethyl)-bicyclo(2.2.2)octan-2-yl)-5Z-hexenoic acid (ONO-8711), the PGE receptor (EP)1 antagonist, as well as indomethacin and potentiated by both vinpocetine and zaprinast at doses that had no effect by themselves on the basal secretion, whereas other subtype-selective PDE inhibitors had no effect. NOR-3 increased the mucosal PGE 2 content in a methylene blueinhibitable manner. These results suggest that NO stimulates gastric HCO 3 Ϫ secretion mediated intracellularly by cGMP and modified by both PDE1 and PDE5, and this response is finally mediated by endogenous PGE 2 via the activation of EP1 receptors.

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Section: Discussionsupporting

confidence: 65%

Section: Discussionmentioning

confidence: 92%

Section: Methodsmentioning

confidence: 99%

Section: The Secretion Of Hcomentioning

confidence: 99%

See 2 more Smart Citations

Phosphodiesterase Isozymes Involved in Regulation of Secretion in Isolated Mouse Stomach in Vitro

Kita

Takahashi²,

Ohashi³

et al. 2008

J Pharmacol Exp Ther

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“…Tuo et al (2007) demonstrated that PGE 2 -stimulated duodenal HCO 3 2 secretion was reduced by the cAMP-dependent signaling pathway inhibitors MDL-12330A (an AC inhibitor) and KT-5720 (a PKA inhibitor) by 23 and 20%, respectively; reduced by the Ca 2+ -influx inhibitor verapamil by 26%; reduced by the calmodulin antagonist W-13 by 24%; and reduced by the PI3K inhibitors wortmannin and LY-294002 by 51 and 47%, respectively. Similarly, elevation of intracellular cAMP levels by the nonselective PDE inhibitor 3-isobutyl-1-methylxanthine, the PDE1 inhibitor vinpocetine, and the PDE3 inhibitor cilostamide increased HCO 3 2 secretion in duodenal mucosa (Hayashi et al, 2007;Takeuchi et al, 2011Takeuchi et al, , 1997.…”

Section: Other Immune Cellsmentioning

confidence: 95%

The Prostanoid EP4 Receptor and Its Signaling Pathway

Yokoyama

Iwatsubo²,

Umemura³

et al. 2013

Pharmacol Rev

223

257

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Receptor guanylyl cyclase C (GC-C): regulation and signal transduction

2009

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Receptor guanylyl cyclase C (GC-C) is the target for the gastrointestinal hormones, guanylin, and uroguanylin as well as the bacterial heat-stable enterotoxins. The major site of expression of GC-C is in the gastrointestinal tract, although this receptor and its ligands play a role in ion secretion in other tissues as well. GC-C shares the domain organization seen in other members of the family of receptor guanylyl cyclases, though subtle differences highlight some of the unique features of GC-C. Gene knock outs in mice for GC-C or its ligands do not lead to embryonic lethality, but modulate responses of these mice to stable toxin peptides, dietary intake of salts, and development and differentiation of intestinal cells. It is clear that there is much to learn in future about the role of this evolutionarily conserved receptor, and its properties in intestinal and extra-intestinal tissues.

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Phosphodiesterase isozymes involved in regulation of HCO3− secretion in isolated mouse duodenum in vitro

Cited by 12 publications

References 20 publications

Phosphodiesterase Isozymes Involved in Regulation of Secretion in Isolated Mouse Stomach in Vitro

Phosphodiesterase Isozymes Involved in Regulation of Secretion in Isolated Mouse Stomach in Vitro

The Prostanoid EP4 Receptor and Its Signaling Pathway

Receptor guanylyl cyclase C (GC-C): regulation and signal transduction

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