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Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation

We previously reported that maternal separation, rat model of early life stress, enhances pressor responses to acute and chronic stressors. The aims of this study were to determine whether Dahl salt-sensitive (DS) rats subjected to maternal separation (MatSep-DS) as compared to normally reared DS (C...

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Autores principales: Loria, Analia S, Pollock, David M, Pollock, Jennifer S
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BlackWell Publishing Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4463836/
https://www.ncbi.nlm.nih.gov/pubmed/25999404
http://dx.doi.org/10.14814/phy2.12408
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author Loria, Analia S
Pollock, David M
Pollock, Jennifer S
author_facet Loria, Analia S
Pollock, David M
Pollock, Jennifer S
author_sort Loria, Analia S
collection PubMed
description We previously reported that maternal separation, rat model of early life stress, enhances pressor responses to acute and chronic stressors. The aims of this study were to determine whether Dahl salt-sensitive (DS) rats subjected to maternal separation (MatSep-DS) as compared to normally reared DS (Ctl-DS) rats show exaggerated blood pressure responses to acute behavioral stressors, such as restraint stress or air jet stress (AJS), or, hypertensive stimuli including chronic high-salt diet (4% NaCl) and angiotensin II (AngII) infusion (200 ng/Kg/min) during 1 week. MatSep was performed in male DS rats for 3 h/day from postnatal days 2–14. At 8 weeks of age, rats were implanted with telemetry transmitters and allowed to recover. Mean arterial pressure (MAP) was not different between MatSep-DS and Ctl-DS rats at baseline (120 ± 2 mmHg vs. 118 ± 1 mmHg, n = 4–8). Blood pressure responses during AJS and restraint stress were not different between MatSep-DS and Ctl-DS at 3 min. However, blood pressure recovery from AJS was significantly impaired in MatSep-DS rats compared to Ctl-DS rats (P < 0.05). 3-h stress-induced similar responses in MatSep and Ctl-DS rats. Chronic blood pressure responses to AngII infusion in rats fed a high-salt diet displayed enhanced MAP in MatSep-DS when compared with Ctl-DS rats (167 ± 5 mmHg vs. 152 ± 2 mmHg, p(interaction) <0.05). However, MAP increased similarly in both groups in response to AngII infusion or high-salt diet separately. Renal parameters such as proteinuria, urine flow rate, and urine electrolytes were not different between groups in response to each treatment. In summary, salt sensitivity induces exaggerated blood pressor responses only in presence of AngII due to early life stress.
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spelling pubmed-44638362015-06-16 Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation Loria, Analia S Pollock, David M Pollock, Jennifer S Physiol Rep Original Research We previously reported that maternal separation, rat model of early life stress, enhances pressor responses to acute and chronic stressors. The aims of this study were to determine whether Dahl salt-sensitive (DS) rats subjected to maternal separation (MatSep-DS) as compared to normally reared DS (Ctl-DS) rats show exaggerated blood pressure responses to acute behavioral stressors, such as restraint stress or air jet stress (AJS), or, hypertensive stimuli including chronic high-salt diet (4% NaCl) and angiotensin II (AngII) infusion (200 ng/Kg/min) during 1 week. MatSep was performed in male DS rats for 3 h/day from postnatal days 2–14. At 8 weeks of age, rats were implanted with telemetry transmitters and allowed to recover. Mean arterial pressure (MAP) was not different between MatSep-DS and Ctl-DS rats at baseline (120 ± 2 mmHg vs. 118 ± 1 mmHg, n = 4–8). Blood pressure responses during AJS and restraint stress were not different between MatSep-DS and Ctl-DS at 3 min. However, blood pressure recovery from AJS was significantly impaired in MatSep-DS rats compared to Ctl-DS rats (P < 0.05). 3-h stress-induced similar responses in MatSep and Ctl-DS rats. Chronic blood pressure responses to AngII infusion in rats fed a high-salt diet displayed enhanced MAP in MatSep-DS when compared with Ctl-DS rats (167 ± 5 mmHg vs. 152 ± 2 mmHg, p(interaction) <0.05). However, MAP increased similarly in both groups in response to AngII infusion or high-salt diet separately. Renal parameters such as proteinuria, urine flow rate, and urine electrolytes were not different between groups in response to each treatment. In summary, salt sensitivity induces exaggerated blood pressor responses only in presence of AngII due to early life stress. BlackWell Publishing Ltd 2015-05-21 /pmc/articles/PMC4463836/ /pubmed/25999404 http://dx.doi.org/10.14814/phy2.12408 Text en © 2015 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society. http://creativecommons.org/licenses/by/4.0/ This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
Loria, Analia S
Pollock, David M
Pollock, Jennifer S
Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation
title Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation
title_full Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation
title_fullStr Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation
title_full_unstemmed Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation
title_short Angiotensin II is required to induce exaggerated salt sensitivity in Dahl rats exposed to maternal separation
title_sort angiotensin ii is required to induce exaggerated salt sensitivity in dahl rats exposed to maternal separation
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4463836/
https://www.ncbi.nlm.nih.gov/pubmed/25999404
http://dx.doi.org/10.14814/phy2.12408
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