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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
Main Authors: Zanella, Regis C., Melo, Mariana Rosso, Furuya, Werner Issao, Colombari, Eduardo, Menani, José V., Colombari, Débora Simões Almeida
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container_title Neuroscience letters
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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
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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&lt;0.05), natriuresis (769±93, vs. PBS: 1158±168μEq/120min, p&lt;0.05) and diuresis (4.1±0.5, vs. PBS: 5.0±0.5ml/120min, p&lt;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. 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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&lt;0.05), natriuresis (769±93, vs. PBS: 1158±168μEq/120min, p&lt;0.05) and diuresis (4.1±0.5, vs. PBS: 5.0±0.5ml/120min, p&lt;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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