Expression of inducible nitric oxide synthase in the lower esophageal sphincter of the endotoxemic opossum

Hyojin Park, Eugene Clark, Joseph J. Cullen, John G. Koland, Myong Soo Kim, Jeffrey L. Conklin

Research output: Contribution to journalArticle

4 Citations (Scopus)

Abstract

Background. Endotoxin modulates esophageal motor function by increasing nitric oxide (NO) production. The aims of this study were to examine inducible nitric oxide synthase (iNOS) induction in the lower esophageal sphincter (LES) of endotoxemic opossums and to investigate the effects of aminoguanidine (AG), a selective inhibitor of iNOS, on plasma nitrite/nitrate levels and on iNOS protein and mRNA expression after exposure to lipopolysaccharide (LPS). Methods. Before and 12h after the intravenous administration of LPS and/or AG, plasma nitrite/nitrate levels were determined. The iNOS protein and mRNA expression were investigated in the tissues taken from the LES by Western blot and reverse-transcriptase polymerase chain reaction (RT-PCR). Results. Plasma nitrite/nitrate levels were significantly increased by LPS. The increase in plasma nitrite/nitrate produced by LPS was significantly decreased by AG. Western blot and RT-PCR demonstrated that iNOS expression was markedly increased by LPS, and attenuated slightly by AG. Conclusions. These studies support the hypothesis that endotoxin increases NO production by the induction of iNOS protein and mRNA.

Original languageEnglish
Pages (from-to)1000-1004
Number of pages5
JournalJournal of Gastroenterology
Volume37
Issue number12
DOIs
Publication statusPublished - 2002 Dec 1

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Opossums
Lower Esophageal Sphincter
Nitric Oxide Synthase Type II
Lipopolysaccharides
Nitrites
Nitrates
Reverse Transcriptase Polymerase Chain Reaction
Endotoxins
Messenger RNA
Nitric Oxide
Western Blotting
Proteins
Intravenous Administration
pimagedine

All Science Journal Classification (ASJC) codes

  • Gastroenterology

Cite this

Park, Hyojin ; Clark, Eugene ; Cullen, Joseph J. ; Koland, John G. ; Kim, Myong Soo ; Conklin, Jeffrey L. / Expression of inducible nitric oxide synthase in the lower esophageal sphincter of the endotoxemic opossum. In: Journal of Gastroenterology. 2002 ; Vol. 37, No. 12. pp. 1000-1004.
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abstract = "Background. Endotoxin modulates esophageal motor function by increasing nitric oxide (NO) production. The aims of this study were to examine inducible nitric oxide synthase (iNOS) induction in the lower esophageal sphincter (LES) of endotoxemic opossums and to investigate the effects of aminoguanidine (AG), a selective inhibitor of iNOS, on plasma nitrite/nitrate levels and on iNOS protein and mRNA expression after exposure to lipopolysaccharide (LPS). Methods. Before and 12h after the intravenous administration of LPS and/or AG, plasma nitrite/nitrate levels were determined. The iNOS protein and mRNA expression were investigated in the tissues taken from the LES by Western blot and reverse-transcriptase polymerase chain reaction (RT-PCR). Results. Plasma nitrite/nitrate levels were significantly increased by LPS. The increase in plasma nitrite/nitrate produced by LPS was significantly decreased by AG. Western blot and RT-PCR demonstrated that iNOS expression was markedly increased by LPS, and attenuated slightly by AG. Conclusions. These studies support the hypothesis that endotoxin increases NO production by the induction of iNOS protein and mRNA.",
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Expression of inducible nitric oxide synthase in the lower esophageal sphincter of the endotoxemic opossum. / Park, Hyojin; Clark, Eugene; Cullen, Joseph J.; Koland, John G.; Kim, Myong Soo; Conklin, Jeffrey L.

In: Journal of Gastroenterology, Vol. 37, No. 12, 01.12.2002, p. 1000-1004.

Research output: Contribution to journalArticle

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AU - Clark, Eugene

AU - Cullen, Joseph J.

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AU - Kim, Myong Soo

AU - Conklin, Jeffrey L.

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N2 - Background. Endotoxin modulates esophageal motor function by increasing nitric oxide (NO) production. The aims of this study were to examine inducible nitric oxide synthase (iNOS) induction in the lower esophageal sphincter (LES) of endotoxemic opossums and to investigate the effects of aminoguanidine (AG), a selective inhibitor of iNOS, on plasma nitrite/nitrate levels and on iNOS protein and mRNA expression after exposure to lipopolysaccharide (LPS). Methods. Before and 12h after the intravenous administration of LPS and/or AG, plasma nitrite/nitrate levels were determined. The iNOS protein and mRNA expression were investigated in the tissues taken from the LES by Western blot and reverse-transcriptase polymerase chain reaction (RT-PCR). Results. Plasma nitrite/nitrate levels were significantly increased by LPS. The increase in plasma nitrite/nitrate produced by LPS was significantly decreased by AG. Western blot and RT-PCR demonstrated that iNOS expression was markedly increased by LPS, and attenuated slightly by AG. Conclusions. These studies support the hypothesis that endotoxin increases NO production by the induction of iNOS protein and mRNA.

AB - Background. Endotoxin modulates esophageal motor function by increasing nitric oxide (NO) production. The aims of this study were to examine inducible nitric oxide synthase (iNOS) induction in the lower esophageal sphincter (LES) of endotoxemic opossums and to investigate the effects of aminoguanidine (AG), a selective inhibitor of iNOS, on plasma nitrite/nitrate levels and on iNOS protein and mRNA expression after exposure to lipopolysaccharide (LPS). Methods. Before and 12h after the intravenous administration of LPS and/or AG, plasma nitrite/nitrate levels were determined. The iNOS protein and mRNA expression were investigated in the tissues taken from the LES by Western blot and reverse-transcriptase polymerase chain reaction (RT-PCR). Results. Plasma nitrite/nitrate levels were significantly increased by LPS. The increase in plasma nitrite/nitrate produced by LPS was significantly decreased by AG. Western blot and RT-PCR demonstrated that iNOS expression was markedly increased by LPS, and attenuated slightly by AG. Conclusions. These studies support the hypothesis that endotoxin increases NO production by the induction of iNOS protein and mRNA.

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