Dilatation and constriction of rat gastric mucosal microvessels through prostaglandin EP<sub>2</sub> and EP<sub>3</sub> receptors

Ohno, Takashi; Katori, Makoto; Murakami, Masataka; Saeki, Takao; Boku, Katsuharu; Nishiyama, Kazuo; Hayashi, Hiromi; Saigenji, Katsunori

doi:10.1046/j.1365-2036.1999.00577.x

Cited by 20 publications

(6 citation statements)

References 37 publications

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“…Thus, there might be different mechanisms involved in adaptive gastric protection, depending on what kinds of mild irritants used. On the other hand, Ohno et al [26]reported that the gastric vasodilatory effect of PGE 2 is mediated by EP2 receptors. We also previously reported that butaprost the EP2 agonist increased GMBF [4].…”

Section: Discussionmentioning

confidence: 99%

Prostaglandin E Receptor EP1 Subtype but Not Prostacyclin IP Receptor Involved in Mucosal Blood Flow Response of Mouse Stomachs following Barrier Disruption

Komoike¹,

Nakashima²,

Nakagiri³

et al. 2003

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Aim: We investigated the role of prostacyclin IP receptors in gastric mucosal protection as well as functional responses induced by taurocholate Na (TC) as a mild irritant using IP receptor knockout mice, in comparison with prostaglandin (PG) E receptor EP1 subtype knockout animals. Methods: Male C57/BL6 mice fasted for 18 h were used under urethane anesthesia. The stomach mounted on an ex vivo chamber was perfused with 20 mM HCl, and the transmucosal potential difference (PD), luminal acid loss, and gastric blood flow (GMBF) were simultaneously measured before and after exposure of the stomach to 20 mM TC for 20 min. Results: Mucosal exposure to TC in wild-type mice caused a marked decrease in PD, followed by an increase in H⁺ loss and GMBF. The PD gradually normalized after removal of TC from the chamber, with minimal damage in the mucosa 1 h later. The increase of GMBF following TC treatment was inhibited by indomethacin with no change in PD reduction or H⁺ loss, resulting in severe lesions in the mucosa. None of these responses induced by TC were significantly altered in IP receptor knockout mice. However, in mice lacking EP1 receptors, TC did not increase GMBF, despite causing PD reduction and acid loss, and resulted in severe damage in the mucosa. Mucosal PGE₂ levels were significantly increased after TC, similarly, in all groups of mice, while levels of 6-keto-PGF_1α showed a slight but not significant increase in all groups. Conclusion: We confirmed the importance of endogenous PGs and EP1 receptors in the adaptive protection and functional responses induced by a mild irritant in mouse stomach and further suggested that IP receptors are not actively involved in maintaining the gastric mucosal integrity under adverse conditions.

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Section: Discussionmentioning

confidence: 99%

Prostaglandin E Receptor EP1 Subtype but Not Prostacyclin IP Receptor Involved in Mucosal Blood Flow Response of Mouse Stomachs following Barrier Disruption

Komoike¹,

Nakashima²,

Nakagiri³

et al. 2003

Digestion

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“…PGE 2 has been reported to stimulate cAMP formation in many tissues, including intestine, microdissected renal tubule segments, and uterus via butaprost sensitive and insensitive receptors [14,26-29]. The mRNA expression results are consistent with these functional studies and suggest that the EP 2 receptor plays important roles in mediating PGE2 stimulated cAMP generation in these tissues [14,21,26-33]. …”

Section: Discussionmentioning

confidence: 53%

Cloning and expression of the rabbit prostaglandin EP2 receptor

et al. 2002

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“…3). Our previous report (22) revealed that constriction of collecting venules and venules may be explained by the action of endogenous PG, such as PGE 2 which may stimulate EP3 receptor signaling. By contrast, collecting venule constriction by ethanol was not enhanced by 1 M NaCl pretreatment but was inhibited instead.…”

Section: Discussionmentioning

confidence: 97%

Mild irritant prevents ethanol-induced gastric mucosal microcirculatory disturbances through actions of calcitonin gene-related peptide and PGI₂in rats

Saeki

Ohno

Kamata

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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Pretreatment with a mild irritant such as 1 M NaCl prevented ethanol-induced mucosal injury, which was abolished by indomethacin, suggesting involvement of endogenous PGs. With the use of intravital microscopy, we investigated the mechanism in microcirculation whereby a mild irritant prevents ethanol-induced mucosal injury. Microcirculation of the basal part of gastric mucosa in anesthetized rats was observed through a window with transillumination. Diameters of arterioles, collecting venules, and venules were measured with an electric microscaler. One molar NaCl alone caused dilation of arterioles and constrictions of collecting venules and venules, which were inhibited by indomethacin. Ethanol (50%) applied to mucosa constricted collecting venules and venules but dilated arterioles. Constriction of collecting venules resulted in mucosal congestion. Pretreatment with 1 M NaCl inhibited ethanol-induced constrictions of collecting venules and venules, and administration of indomethacin or a calcitonin gene-related peptide (CGRP) antagonist, CGRP-(8-37), abolished elimination of constrictions. Topical application (1 nM-10 microM) of PGE2 or beraprost sodium (a PGI2 analog) to microvasculature markedly and dose-dependently dilated arterioles, whereas that of PGE2, but not beraprost, slightly constricted collecting venules. Pretreatment of microvasculature with a nonvasoactive concentration of PGE2 (100 nM) or beraprost (1 nM) completely inhibited ethanol-induced constriction of collecting venules. The inhibitory effect of beraprost but not of PGE2 was abolished by CGRP-(8-37). Present results suggest that the mechanism whereby 1 M NaCl prevents ethanol-induced injury is elimination of constrictions of collecting venules and venules by CGRP whose release may be enhanced by PGI2 but not by PGE2.

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Dilatation and constriction of rat gastric mucosal microvessels through prostaglandin EP₂ and EP₃ receptors

Abstract: These results suggest that PGE2 dilated both arterioles and venules in the rat gastric mucosa through the EP2 receptors and constricted the venules through the EP3 receptors.

Cited by 20 publications

References 37 publications

Prostaglandin E Receptor EP1 Subtype but Not Prostacyclin IP Receptor Involved in Mucosal Blood Flow Response of Mouse Stomachs following Barrier Disruption

Prostaglandin E Receptor EP1 Subtype but Not Prostacyclin IP Receptor Involved in Mucosal Blood Flow Response of Mouse Stomachs following Barrier Disruption

Cloning and expression of the rabbit prostaglandin EP2 receptor

Mild irritant prevents ethanol-induced gastric mucosal microcirculatory disturbances through actions of calcitonin gene-related peptide and PGI₂in rats

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Dilatation and constriction of rat gastric mucosal microvessels through prostaglandin EP2 and EP3 receptors

Abstract: These results suggest that PGE2 dilated both arterioles and venules in the rat gastric mucosa through the EP2 receptors and constricted the venules through the EP3 receptors.

Cited by 20 publications

References 37 publications

Prostaglandin E Receptor EP1 Subtype but Not Prostacyclin IP Receptor Involved in Mucosal Blood Flow Response of Mouse Stomachs following Barrier Disruption

Prostaglandin E Receptor EP1 Subtype but Not Prostacyclin IP Receptor Involved in Mucosal Blood Flow Response of Mouse Stomachs following Barrier Disruption

Cloning and expression of the rabbit prostaglandin EP2 receptor

Mild irritant prevents ethanol-induced gastric mucosal microcirculatory disturbances through actions of calcitonin gene-related peptide and PGI2in rats

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Dilatation and constriction of rat gastric mucosal microvessels through prostaglandin EP₂ and EP₃ receptors

Mild irritant prevents ethanol-induced gastric mucosal microcirculatory disturbances through actions of calcitonin gene-related peptide and PGI₂in rats