Stimulation by Prostaglandin E2 of Alkaline Secretion in the Rat Duodenum: Comparative Study with Hypertonic NaCI

Takeuchi, Koji; Niida, Hiromichi; Takinami, Yusuke; Okabe, Susumu

doi:10.1254/jjp.53.67

Cited by 3 publications

(1 citation statement)

References 16 publications

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“…The net increase of HC03 output caused by PGE2 (100 ag/kg, i.v.) was about 8 ,uEq/rat, which was equivalent to that obtained by 300 ,ug/kg of this agent given s.c. (17). The dura tion of stimulation after i.v.…”

Section: Discussionmentioning

confidence: 99%

Determination of bicarbonate output using pH deflection in the rat duodenum: Influences of prostaglandins and cholinergic agents.

et al. 1990

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Abstract-We set up a system to measure the luminal pH, potential difference (PD) and bicarbonate output in the anesthetized rat duodenum, and investigated these responses caused by prostaglandins (PGs) and cholinergic agents. When the proximal duodenum (1.7 cm) was perfused at a flow rate of 0.7 ml/min with saline adjusted to pH 4.5, the duodenal pH, PD and HC03 output were 5.5 to 6.0, -4 to -6 mV and 1 .2 to 1.6 aEq/10 min, respectively; they were markedly reduced by i.v.injection of saturated KCI. Both natural (PGE1, PGE2) and synthetic (PGE2, PG12) PGs, given either s.c. or i.v., significantly elevated all these parameters, while indomethacin (s.c.) decreased the pH as well as the PD. Small but significant increases of the pH were observed after i.v. administration of cholinergic agents (carbachol, hethanechol), a GABAergic agent (baclofen) and an analogue of thyrotropin releasing hormone (YM-14673), with a temporal elevation of the PD; the degree of net HC03 output caused by these agents was 20-50% of the values obtained with PGE2 (100 ,ug/kg, i.v.), and they were significantly reduced in the presence of atropine. These results suggest that (a) the system using pH deflections can be used to sensitively detect HC03 output in the rat duodenum, and (b) duodenal acid neutralizing capacity may be regulated by central and peripheral cholinergic systems as well as endogenous PGs.

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Section: Discussionmentioning

confidence: 99%

Determination of bicarbonate output using pH deflection in the rat duodenum: Influences of prostaglandins and cholinergic agents.

et al. 1990

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Determination of gastroduodenal alkaline responses in the rat

Takeuchi

Niida

Ueshima

et al. 1990

Journal of Pharmacological Methods

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Stimulatory Effect of Nitric Oxide on Bicarbonate Secretion in Bullfrog Duodenums in vitro

Furukawa

Kitamura²,

Sugamoto³

et al. 1999

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The effect of nitric oxide (NO) on HCO^–₃ secretion was examined in vitro using an isolated preparation of bullfrog duodenum. The tissue was bathed in unbuffered Ringer’s solution gassed with 100% O₂ on the mucosal side and HCO^–₃ Ringer’s solution gassed with 95% O₂–5% CO₂ on the serosal side. The HCO^–₃ secretion was measured by the pH-stat method using 2 mmol/l HCl as the titrant to keep the mucosal pH at 7.4. (±)-(E)-Ethyl-2-[(E)-hydroxyimino]-5-nitro-3-hexenamine (NOR3) was used as a NO donor and added to the serosal solution. To analyze the NOR3 action on HCO^–₃ secretion, the effects of dibutyryl adenosine-3′,5′-cyclic monophosphate (dbcAMP), dibutyryl guanosine-3′,5′-cyclic monophosphate (dbcGMP), methylene blue, and indomethacin on the HCO^–₃ response were also examined. NOR3 (1×10^–4 and 3×10^–4 mol/l) caused an increase in HCO^–₃ secretion in a dose-dependent manner, and this effect appeared with an about 30-min time lag, reaching the level of 1.5–2.5 times greater than basal values at 1–2 h later. Both dbcAMP (1×10^–3 mol/l) and dbcGMP (1×10^–3 mol/l) also caused a significant increase in HCO^–₃ secretion in bullfrog duodenums in vitro, although the onset of the HCO^–₃ response to dbcGMP was delayed as compared to the former. The stimulatory action of NOR3 on duodenal HCO^–₃ secretion was significantly attenuated by methylene blue (5×10^–5 mol/l) and indomethacin (1×10^–5 mol/l), the latter also inhibiting the HCO^–₃ response to dbcGMP. The release of prostaglandin E₂ in the serosal solution was significantly increased after addition of NOR3 (3×10^–4 mol/l) and dbcGMP (1×10^–3 mol/l) in an indomethacin-sensitive manner. These results suggest that the NO donor increases duodenal HCO^–₃ secretion in vitro, and this action of NO donor is cGMP-dependent and mediated by endogenous prostaglandins. Duodenal HCO^–₃ secretion may be regulated locally by NO/cGMP in addition to prostaglandin/cAMP.

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Stimulation by Prostaglandin E2 of Alkaline Secretion in the Rat Duodenum: Comparative Study with Hypertonic NaCI

Cited by 3 publications

References 16 publications

Determination of bicarbonate output using pH deflection in the rat duodenum: Influences of prostaglandins and cholinergic agents.

Determination of bicarbonate output using pH deflection in the rat duodenum: Influences of prostaglandins and cholinergic agents.

Determination of gastroduodenal alkaline responses in the rat

Stimulatory Effect of Nitric Oxide on Bicarbonate Secretion in Bullfrog Duodenums in vitro

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