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Regulation of electrolyte transport by nitric oxide in the mouse cecum
The effect and role of nitric oxide (NO) in the regulation of ion transport in the mouse cecum were investigated. l-arginine, used to increase NO production, increased short-circuit current ( I sc), a measure of ion transport, in a concentration-dependent manner with a maximal increase of 193.8±65.5...
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Published in: | European journal of pharmacology 1998-05, Vol.350 (1), p.93-99 |
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creator | Homaidan, Fadia R Martello, Laura A Melson, Stephen J Robert Burakoff |
description | The effect and role of nitric oxide (NO) in the regulation of ion transport in the mouse cecum were investigated.
l-arginine, used to increase NO production, increased short-circuit current (
I
sc), a measure of ion transport, in a concentration-dependent manner with a maximal increase of 193.8±65.5
μA/cm
2. This increase was not changed in Cl
−- or HCO
3
−-free buffers, but was significantly decreased in Na
+-free buffer. Using immunohistochemistry, the constitutive form of nitric oxide synthase was found not to be different in the inflamed cecum. The inducible form of the enzyme, however, which was absent in the cecum of normal mice, was present in high levels in the cecum of the colitic mouse. These results suggest that NO causes an increase in Na
+ absorption. The increased levels of inducible NO synthase in the inflamed cecum suggest a role for NO in the pathophysiology of inflammatory bowel disease. |
doi_str_mv | 10.1016/S0014-2999(98)00221-0 |
format | article |
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l-arginine, used to increase NO production, increased short-circuit current (
I
sc), a measure of ion transport, in a concentration-dependent manner with a maximal increase of 193.8±65.5
μA/cm
2. This increase was not changed in Cl
−- or HCO
3
−-free buffers, but was significantly decreased in Na
+-free buffer. Using immunohistochemistry, the constitutive form of nitric oxide synthase was found not to be different in the inflamed cecum. The inducible form of the enzyme, however, which was absent in the cecum of normal mice, was present in high levels in the cecum of the colitic mouse. These results suggest that NO causes an increase in Na
+ absorption. The increased levels of inducible NO synthase in the inflamed cecum suggest a role for NO in the pathophysiology of inflammatory bowel disease.</description><identifier>ISSN: 0014-2999</identifier><identifier>EISSN: 1879-0712</identifier><identifier>DOI: 10.1016/S0014-2999(98)00221-0</identifier><identifier>PMID: 9683020</identifier><identifier>CODEN: EJPHAZ</identifier><language>eng</language><publisher>Amsterdam: Elsevier B.V</publisher><subject>Animals ; Arginine - pharmacology ; Biological and medical sciences ; Biological Transport ; Cecum ; Cecum - metabolism ; Cell physiology ; Colitis - enzymology ; Colitis - metabolism ; Disease Models, Animal ; Electrolytes - metabolism ; Female ; Fundamental and applied biological sciences. Psychology ; Immunohistochemistry ; Inflammatory bowel disease ; Ion transport ; Membrane and intracellular transports ; Mice ; Mice, Inbred C3H ; Molecular and cellular biology ; Neurons - drug effects ; Nitric oxide (NO) ; Nitric Oxide - metabolism ; Nitric Oxide Synthase - metabolism ; Nitric Oxide Synthase Type II ; Short-circuit current</subject><ispartof>European journal of pharmacology, 1998-05, Vol.350 (1), p.93-99</ispartof><rights>1998 Elsevier Science B.V.</rights><rights>1998 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c436t-ac5720d14bd067d3bcf4394d5bdf0f2dbd937c754c0eb834cde0879fc3799bb73</citedby><cites>FETCH-LOGICAL-c436t-ac5720d14bd067d3bcf4394d5bdf0f2dbd937c754c0eb834cde0879fc3799bb73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2381529$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9683020$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Homaidan, Fadia R</creatorcontrib><creatorcontrib>Martello, Laura A</creatorcontrib><creatorcontrib>Melson, Stephen J</creatorcontrib><creatorcontrib>Robert Burakoff</creatorcontrib><title>Regulation of electrolyte transport by nitric oxide in the mouse cecum</title><title>European journal of pharmacology</title><addtitle>Eur J Pharmacol</addtitle><description>The effect and role of nitric oxide (NO) in the regulation of ion transport in the mouse cecum were investigated.
l-arginine, used to increase NO production, increased short-circuit current (
I
sc), a measure of ion transport, in a concentration-dependent manner with a maximal increase of 193.8±65.5
μA/cm
2. This increase was not changed in Cl
−- or HCO
3
−-free buffers, but was significantly decreased in Na
+-free buffer. Using immunohistochemistry, the constitutive form of nitric oxide synthase was found not to be different in the inflamed cecum. The inducible form of the enzyme, however, which was absent in the cecum of normal mice, was present in high levels in the cecum of the colitic mouse. These results suggest that NO causes an increase in Na
+ absorption. The increased levels of inducible NO synthase in the inflamed cecum suggest a role for NO in the pathophysiology of inflammatory bowel disease.</description><subject>Animals</subject><subject>Arginine - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Biological Transport</subject><subject>Cecum</subject><subject>Cecum - metabolism</subject><subject>Cell physiology</subject><subject>Colitis - enzymology</subject><subject>Colitis - metabolism</subject><subject>Disease Models, Animal</subject><subject>Electrolytes - metabolism</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Immunohistochemistry</subject><subject>Inflammatory bowel disease</subject><subject>Ion transport</subject><subject>Membrane and intracellular transports</subject><subject>Mice</subject><subject>Mice, Inbred C3H</subject><subject>Molecular and cellular biology</subject><subject>Neurons - drug effects</subject><subject>Nitric oxide (NO)</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Nitric Oxide Synthase Type II</subject><subject>Short-circuit current</subject><issn>0014-2999</issn><issn>1879-0712</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</creationdate><recordtype>article</recordtype><recordid>eNqFkE1r3DAQhkVpSTZpf0JAh1CSg5uR5C-dQgn5gkAhbc_CGo1bFdvaSHLp_vt6s8tec5rDPO98PIydCfgiQNRX3wFEWUit9YVuLwGkFAW8YyvRNrqARsj3bHVAjtlJSn8AoNKyOmJHum4VSFixu2f6NQ9d9mHioec0EOYYhk0mnmM3pXWImdsNn3yOHnn45x1xP_H8m_gY5kQcCefxI_vQd0OiT_t6yn7e3f64eSievt0_3nx9KrBUdS46rBoJTpTWQd04ZbEvlS5dZV0PvXTWadVgU5UIZFtVoiNY3ulRNVpb26hT9nk3dx3Dy0wpm9EnpGHoJlquMS2AgrrWC1jtQIwhpUi9WUc_dnFjBJitP_Pqz2zlGN2aV38GltzZfsFsR3KH1F7Y0j_f97uE3dAvjtCnAyZVKyq5XX-9w2iR8ddTNAk9TUjOx8WwccG_cch_hmGMzg</recordid><startdate>19980529</startdate><enddate>19980529</enddate><creator>Homaidan, Fadia R</creator><creator>Martello, Laura A</creator><creator>Melson, Stephen J</creator><creator>Robert Burakoff</creator><general>Elsevier B.V</general><general>Elsevier</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19980529</creationdate><title>Regulation of electrolyte transport by nitric oxide in the mouse cecum</title><author>Homaidan, Fadia R ; Martello, Laura A ; Melson, Stephen J ; Robert Burakoff</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c436t-ac5720d14bd067d3bcf4394d5bdf0f2dbd937c754c0eb834cde0879fc3799bb73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Arginine - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Biological Transport</topic><topic>Cecum</topic><topic>Cecum - metabolism</topic><topic>Cell physiology</topic><topic>Colitis - enzymology</topic><topic>Colitis - metabolism</topic><topic>Disease Models, Animal</topic><topic>Electrolytes - metabolism</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Immunohistochemistry</topic><topic>Inflammatory bowel disease</topic><topic>Ion transport</topic><topic>Membrane and intracellular transports</topic><topic>Mice</topic><topic>Mice, Inbred C3H</topic><topic>Molecular and cellular biology</topic><topic>Neurons - drug effects</topic><topic>Nitric oxide (NO)</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Nitric Oxide Synthase Type II</topic><topic>Short-circuit current</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Homaidan, Fadia R</creatorcontrib><creatorcontrib>Martello, Laura A</creatorcontrib><creatorcontrib>Melson, Stephen J</creatorcontrib><creatorcontrib>Robert Burakoff</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of pharmacology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Homaidan, Fadia R</au><au>Martello, Laura A</au><au>Melson, Stephen J</au><au>Robert Burakoff</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of electrolyte transport by nitric oxide in the mouse cecum</atitle><jtitle>European journal of pharmacology</jtitle><addtitle>Eur J Pharmacol</addtitle><date>1998-05-29</date><risdate>1998</risdate><volume>350</volume><issue>1</issue><spage>93</spage><epage>99</epage><pages>93-99</pages><issn>0014-2999</issn><eissn>1879-0712</eissn><coden>EJPHAZ</coden><abstract>The effect and role of nitric oxide (NO) in the regulation of ion transport in the mouse cecum were investigated.
l-arginine, used to increase NO production, increased short-circuit current (
I
sc), a measure of ion transport, in a concentration-dependent manner with a maximal increase of 193.8±65.5
μA/cm
2. This increase was not changed in Cl
−- or HCO
3
−-free buffers, but was significantly decreased in Na
+-free buffer. Using immunohistochemistry, the constitutive form of nitric oxide synthase was found not to be different in the inflamed cecum. The inducible form of the enzyme, however, which was absent in the cecum of normal mice, was present in high levels in the cecum of the colitic mouse. These results suggest that NO causes an increase in Na
+ absorption. The increased levels of inducible NO synthase in the inflamed cecum suggest a role for NO in the pathophysiology of inflammatory bowel disease.</abstract><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>9683020</pmid><doi>10.1016/S0014-2999(98)00221-0</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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language | eng |
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subjects | Animals Arginine - pharmacology Biological and medical sciences Biological Transport Cecum Cecum - metabolism Cell physiology Colitis - enzymology Colitis - metabolism Disease Models, Animal Electrolytes - metabolism Female Fundamental and applied biological sciences. Psychology Immunohistochemistry Inflammatory bowel disease Ion transport Membrane and intracellular transports Mice Mice, Inbred C3H Molecular and cellular biology Neurons - drug effects Nitric oxide (NO) Nitric Oxide - metabolism Nitric Oxide Synthase - metabolism Nitric Oxide Synthase Type II Short-circuit current |
title | Regulation of electrolyte transport by nitric oxide in the mouse cecum |
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