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Hydrogen peroxide centrally attenuates hyperosmolarity-induced thirst and natriuresis
•Intragastric hypertonic NaCl simulates osmotically active substances ingestion.•Intragastric hypertonic NaCl induces thirst, natriuresis and diuresis.•H2O2 in the brain may modulate behavioral and renal responses.•Central H2O2 decreased hypertonic NaCl-induced thirst and natriuresis.•Central H2O2 a...
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Published in: | Neuroscience letters 2016-01, Vol.610, p.129-134 |
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description | •Intragastric hypertonic NaCl simulates osmotically active substances ingestion.•Intragastric hypertonic NaCl induces thirst, natriuresis and diuresis.•H2O2 in the brain may modulate behavioral and renal responses.•Central H2O2 decreased hypertonic NaCl-induced thirst and natriuresis.•Central H2O2 also decreased meal-associated water intake.
Intragastric hypertonic NaCl that simulates the ingestion of osmotically active substances by food intake induces thirst, vasopressin and oxytocin release, diuresis and natriuresis. Reactive oxygen species (ROS) produced endogenously in central areas may act modulating autonomic and behavioral responses. In the present study, we investigated the effects of H2O2 injected centrally on water intake and renal responses induced by increasing plasma osmolality with intragastric (ig) administration of 2M NaCl (2ml/rat). Male Holtzman rats (280–320g) with stainless steel cannula implanted in the lateral ventricle (LV) were used. Injections of H2O2 (2.5μmol/1μl) into the LV reduced ig 2M NaCl-induced water intake (3.1±0.7, vs. PBS: 8.6±1.0ml/60min, p |
doi_str_mv | 10.1016/j.neulet.2015.10.067 |
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Intragastric hypertonic NaCl that simulates the ingestion of osmotically active substances by food intake induces thirst, vasopressin and oxytocin release, diuresis and natriuresis. Reactive oxygen species (ROS) produced endogenously in central areas may act modulating autonomic and behavioral responses. In the present study, we investigated the effects of H2O2 injected centrally on water intake and renal responses induced by increasing plasma osmolality with intragastric (ig) administration of 2M NaCl (2ml/rat). Male Holtzman rats (280–320g) with stainless steel cannula implanted in the lateral ventricle (LV) were used. Injections of H2O2 (2.5μmol/1μl) into the LV reduced ig 2M NaCl-induced water intake (3.1±0.7, vs. PBS: 8.6±1.0ml/60min, p<0.05), natriuresis (769±93, vs. PBS: 1158±168μEq/120min, p<0.05) and diuresis (4.1±0.5, vs. PBS: 5.0±0.5ml/120min, p<0.05). Injections of H2O2 into the LV also decreased meal associated water intake (4.9±1.5, vs. PBS: 11.0±1.7ml/120min). However, H2O2 into the LV did not modify 2% sucrose intake (3.3±1.5, vs. PBS: 5.4±2.3ml/120min) or 24h food deprivation-induced food intake (8.2±2.0, vs. PBS: 11.0±1.6g/120min), suggesting that this treatment does not produce nonspecific inhibition of ingestive behaviors. The data suggest an inhibitory role for H2O2 acting centrally on thirst and natriuresis induced by hyperosmolarity and on meal-associated thirst.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2015.10.067</identifier><identifier>PMID: 26528792</identifier><language>eng</language><publisher>Ireland: Elsevier Ireland Ltd</publisher><subject>Animals ; Cations, Monovalent ; Drinking - drug effects ; Eating - drug effects ; Hydrogen Peroxide - administration & dosage ; Hydrogen Peroxide - metabolism ; Hydrogen Peroxide - pharmacology ; Hypertonic saline ; Injections, Intraventricular ; Male ; Natriuresis - drug effects ; Osmolar Concentration ; Osmoreceptors ; Potassium - urine ; Rats, Sprague-Dawley ; Reactive oxygen species ; Renal excretion ; Sodium - urine ; Sodium Chloride - pharmacology ; Sucrose ; Thirst - drug effects ; Water intake</subject><ispartof>Neuroscience letters, 2016-01, Vol.610, p.129-134</ispartof><rights>2015 Elsevier Ireland Ltd</rights><rights>Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-cbe922f9b3cde08c7324982009a0dd1d0bf9eb3717511f429691d4121d78eb863</citedby><cites>FETCH-LOGICAL-c362t-cbe922f9b3cde08c7324982009a0dd1d0bf9eb3717511f429691d4121d78eb863</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27900,27901</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26528792$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zanella, Regis C.</creatorcontrib><creatorcontrib>Melo, Mariana Rosso</creatorcontrib><creatorcontrib>Furuya, Werner Issao</creatorcontrib><creatorcontrib>Colombari, Eduardo</creatorcontrib><creatorcontrib>Menani, José V.</creatorcontrib><creatorcontrib>Colombari, Débora Simões Almeida</creatorcontrib><title>Hydrogen peroxide centrally attenuates hyperosmolarity-induced thirst and natriuresis</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>•Intragastric hypertonic NaCl simulates osmotically active substances ingestion.•Intragastric hypertonic NaCl induces thirst, natriuresis and diuresis.•H2O2 in the brain may modulate behavioral and renal responses.•Central H2O2 decreased hypertonic NaCl-induced thirst and natriuresis.•Central H2O2 also decreased meal-associated water intake.
Intragastric hypertonic NaCl that simulates the ingestion of osmotically active substances by food intake induces thirst, vasopressin and oxytocin release, diuresis and natriuresis. Reactive oxygen species (ROS) produced endogenously in central areas may act modulating autonomic and behavioral responses. In the present study, we investigated the effects of H2O2 injected centrally on water intake and renal responses induced by increasing plasma osmolality with intragastric (ig) administration of 2M NaCl (2ml/rat). Male Holtzman rats (280–320g) with stainless steel cannula implanted in the lateral ventricle (LV) were used. Injections of H2O2 (2.5μmol/1μl) into the LV reduced ig 2M NaCl-induced water intake (3.1±0.7, vs. PBS: 8.6±1.0ml/60min, p<0.05), natriuresis (769±93, vs. PBS: 1158±168μEq/120min, p<0.05) and diuresis (4.1±0.5, vs. PBS: 5.0±0.5ml/120min, p<0.05). Injections of H2O2 into the LV also decreased meal associated water intake (4.9±1.5, vs. PBS: 11.0±1.7ml/120min). However, H2O2 into the LV did not modify 2% sucrose intake (3.3±1.5, vs. PBS: 5.4±2.3ml/120min) or 24h food deprivation-induced food intake (8.2±2.0, vs. PBS: 11.0±1.6g/120min), suggesting that this treatment does not produce nonspecific inhibition of ingestive behaviors. The data suggest an inhibitory role for H2O2 acting centrally on thirst and natriuresis induced by hyperosmolarity and on meal-associated thirst.</description><subject>Animals</subject><subject>Cations, Monovalent</subject><subject>Drinking - drug effects</subject><subject>Eating - drug effects</subject><subject>Hydrogen Peroxide - administration & dosage</subject><subject>Hydrogen Peroxide - metabolism</subject><subject>Hydrogen Peroxide - pharmacology</subject><subject>Hypertonic saline</subject><subject>Injections, Intraventricular</subject><subject>Male</subject><subject>Natriuresis - drug effects</subject><subject>Osmolar Concentration</subject><subject>Osmoreceptors</subject><subject>Potassium - urine</subject><subject>Rats, Sprague-Dawley</subject><subject>Reactive oxygen species</subject><subject>Renal excretion</subject><subject>Sodium - urine</subject><subject>Sodium Chloride - pharmacology</subject><subject>Sucrose</subject><subject>Thirst - drug effects</subject><subject>Water intake</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><recordid>eNp9kEtPwzAQhC0EgvL4BwjlyCVl7TwcX5AQ4iVV4gJny7E31FXqFNtB5N_jqoUjp5VmZ3Y1HyGXFOYUaH2zmjsce4xzBrRK0hxqfkBmtOEs54KzQzKDAsq8ECWckNMQVgBQ0ao8JiesrljDBZuR9-fJ-OEDXbZBP3xbg5lGF73q-ylTMaIbVcSQLaftPqyHXnkbp9w6M2o0WVxaH2KmnMmcit6OHoMN5-SoU33Ai_08I--PD2_3z_ni9enl_m6R66JmMdctCsY60RbaIDSaF6wUDQMQCoyhBtpOYFtwyitKu5KJWlBTUkYNb7Bt6uKMXO_ubvzwOWKIcm2Dxr5XDocxyBRkRcpCmazlzqpTjeCxkxtv18pPkoLcApUruQMqt0C3agKaYlf7D2O7RvMX-iWYDLc7A6aeXxa9DNqiS2ysRx2lGez_H34AloiKqQ</recordid><startdate>20160101</startdate><enddate>20160101</enddate><creator>Zanella, Regis C.</creator><creator>Melo, Mariana Rosso</creator><creator>Furuya, Werner Issao</creator><creator>Colombari, Eduardo</creator><creator>Menani, José V.</creator><creator>Colombari, Débora Simões Almeida</creator><general>Elsevier Ireland Ltd</general><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>20160101</creationdate><title>Hydrogen peroxide centrally attenuates hyperosmolarity-induced thirst and natriuresis</title><author>Zanella, Regis C. ; Melo, Mariana Rosso ; Furuya, Werner Issao ; Colombari, Eduardo ; Menani, José V. ; Colombari, Débora Simões Almeida</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-cbe922f9b3cde08c7324982009a0dd1d0bf9eb3717511f429691d4121d78eb863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Cations, Monovalent</topic><topic>Drinking - drug effects</topic><topic>Eating - drug effects</topic><topic>Hydrogen Peroxide - administration & dosage</topic><topic>Hydrogen Peroxide - metabolism</topic><topic>Hydrogen Peroxide - pharmacology</topic><topic>Hypertonic saline</topic><topic>Injections, Intraventricular</topic><topic>Male</topic><topic>Natriuresis - drug effects</topic><topic>Osmolar Concentration</topic><topic>Osmoreceptors</topic><topic>Potassium - urine</topic><topic>Rats, Sprague-Dawley</topic><topic>Reactive oxygen species</topic><topic>Renal excretion</topic><topic>Sodium - urine</topic><topic>Sodium Chloride - pharmacology</topic><topic>Sucrose</topic><topic>Thirst - drug effects</topic><topic>Water intake</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zanella, Regis C.</creatorcontrib><creatorcontrib>Melo, Mariana Rosso</creatorcontrib><creatorcontrib>Furuya, Werner Issao</creatorcontrib><creatorcontrib>Colombari, Eduardo</creatorcontrib><creatorcontrib>Menani, José V.</creatorcontrib><creatorcontrib>Colombari, Débora Simões Almeida</creatorcontrib><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>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zanella, Regis C.</au><au>Melo, Mariana Rosso</au><au>Furuya, Werner Issao</au><au>Colombari, Eduardo</au><au>Menani, José V.</au><au>Colombari, Débora Simões Almeida</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hydrogen peroxide centrally attenuates hyperosmolarity-induced thirst and natriuresis</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2016-01-01</date><risdate>2016</risdate><volume>610</volume><spage>129</spage><epage>134</epage><pages>129-134</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><abstract>•Intragastric hypertonic NaCl simulates osmotically active substances ingestion.•Intragastric hypertonic NaCl induces thirst, natriuresis and diuresis.•H2O2 in the brain may modulate behavioral and renal responses.•Central H2O2 decreased hypertonic NaCl-induced thirst and natriuresis.•Central H2O2 also decreased meal-associated water intake.
Intragastric hypertonic NaCl that simulates the ingestion of osmotically active substances by food intake induces thirst, vasopressin and oxytocin release, diuresis and natriuresis. Reactive oxygen species (ROS) produced endogenously in central areas may act modulating autonomic and behavioral responses. In the present study, we investigated the effects of H2O2 injected centrally on water intake and renal responses induced by increasing plasma osmolality with intragastric (ig) administration of 2M NaCl (2ml/rat). Male Holtzman rats (280–320g) with stainless steel cannula implanted in the lateral ventricle (LV) were used. Injections of H2O2 (2.5μmol/1μl) into the LV reduced ig 2M NaCl-induced water intake (3.1±0.7, vs. PBS: 8.6±1.0ml/60min, p<0.05), natriuresis (769±93, vs. PBS: 1158±168μEq/120min, p<0.05) and diuresis (4.1±0.5, vs. PBS: 5.0±0.5ml/120min, p<0.05). Injections of H2O2 into the LV also decreased meal associated water intake (4.9±1.5, vs. PBS: 11.0±1.7ml/120min). However, H2O2 into the LV did not modify 2% sucrose intake (3.3±1.5, vs. PBS: 5.4±2.3ml/120min) or 24h food deprivation-induced food intake (8.2±2.0, vs. PBS: 11.0±1.6g/120min), suggesting that this treatment does not produce nonspecific inhibition of ingestive behaviors. The data suggest an inhibitory role for H2O2 acting centrally on thirst and natriuresis induced by hyperosmolarity and on meal-associated thirst.</abstract><cop>Ireland</cop><pub>Elsevier Ireland Ltd</pub><pmid>26528792</pmid><doi>10.1016/j.neulet.2015.10.067</doi><tpages>6</tpages></addata></record> |
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subjects | Animals Cations, Monovalent Drinking - drug effects Eating - drug effects Hydrogen Peroxide - administration & dosage Hydrogen Peroxide - metabolism Hydrogen Peroxide - pharmacology Hypertonic saline Injections, Intraventricular Male Natriuresis - drug effects Osmolar Concentration Osmoreceptors Potassium - urine Rats, Sprague-Dawley Reactive oxygen species Renal excretion Sodium - urine Sodium Chloride - pharmacology Sucrose Thirst - drug effects Water intake |
title | Hydrogen peroxide centrally attenuates hyperosmolarity-induced thirst and natriuresis |
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