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Severe food restriction activates the central renin angiotensin system

We previously showed that 2 weeks of a severe food restricted (sFR) diet (40% of the caloric intake of the control (CT) diet) up‐regulated the circulating renin angiotensin (Ang) system (RAS) in female Fischer rats, most likely as a result of the fall in plasma volume. In this study, we investigated...

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Autores principales: De Souza, Aline Maria Arlindo, Linares, Andrea, Speth, Robert C., Campos, Glenda V., Ji, Hong, Chianca, Deoclécio, Sandberg, Kathryn, De Menezes, Rodrigo C. A.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6954120/
https://www.ncbi.nlm.nih.gov/pubmed/31925945
http://dx.doi.org/10.14814/phy2.14338
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author De Souza, Aline Maria Arlindo
Linares, Andrea
Speth, Robert C.
Campos, Glenda V.
Ji, Hong
Chianca, Deoclécio
Sandberg, Kathryn
De Menezes, Rodrigo C. A.
author_facet De Souza, Aline Maria Arlindo
Linares, Andrea
Speth, Robert C.
Campos, Glenda V.
Ji, Hong
Chianca, Deoclécio
Sandberg, Kathryn
De Menezes, Rodrigo C. A.
author_sort De Souza, Aline Maria Arlindo
collection PubMed
description We previously showed that 2 weeks of a severe food restricted (sFR) diet (40% of the caloric intake of the control (CT) diet) up‐regulated the circulating renin angiotensin (Ang) system (RAS) in female Fischer rats, most likely as a result of the fall in plasma volume. In this study, we investigated the role of the central RAS in the mean arterial pressure (MAP) and heart rate (HR) dysregulation associated with sFR. Although sFR reduced basal mean MAP and HR, the magnitude of the pressor response to intracerebroventricular (icv) microinjection of Ang‐[1‐8] was not affected; however, HR was 57 ± 13 bpm lower 26 min after Ang‐[1‐8] microinjection in the sFR rats and a similar response was observed after losartan was microinjected. The major catabolic pathway of Ang‐[1‐8] in the hypothalamus was via Ang‐[1‐7]; however, no differences were detected in the rate of Ang‐[1‐8] synthesis or degradation between CT and sFR animals. While sFR had no effect on the AT(1)R binding in the subfornical organ (SFO), the organum vasculosum laminae terminalis (OVLT) and median preoptic nucleus (MnPO) of the paraventricular anteroventral third ventricle, ligand binding increased 1.4‐fold in the paraventricular nucleus (PVN) of the hypothalamus. These findings suggest that sFR stimulates the central RAS by increasing AT(1)R expression in the PVN as a compensatory response to the reduction in basal MAP and HR. These findings have implications for people experiencing a period of sFR since an activated central RAS could increase their risk of disorders involving over activation of the RAS including renal and cardiovascular diseases.
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spelling pubmed-69541202020-01-14 Severe food restriction activates the central renin angiotensin system De Souza, Aline Maria Arlindo Linares, Andrea Speth, Robert C. Campos, Glenda V. Ji, Hong Chianca, Deoclécio Sandberg, Kathryn De Menezes, Rodrigo C. A. Physiol Rep Original Research We previously showed that 2 weeks of a severe food restricted (sFR) diet (40% of the caloric intake of the control (CT) diet) up‐regulated the circulating renin angiotensin (Ang) system (RAS) in female Fischer rats, most likely as a result of the fall in plasma volume. In this study, we investigated the role of the central RAS in the mean arterial pressure (MAP) and heart rate (HR) dysregulation associated with sFR. Although sFR reduced basal mean MAP and HR, the magnitude of the pressor response to intracerebroventricular (icv) microinjection of Ang‐[1‐8] was not affected; however, HR was 57 ± 13 bpm lower 26 min after Ang‐[1‐8] microinjection in the sFR rats and a similar response was observed after losartan was microinjected. The major catabolic pathway of Ang‐[1‐8] in the hypothalamus was via Ang‐[1‐7]; however, no differences were detected in the rate of Ang‐[1‐8] synthesis or degradation between CT and sFR animals. While sFR had no effect on the AT(1)R binding in the subfornical organ (SFO), the organum vasculosum laminae terminalis (OVLT) and median preoptic nucleus (MnPO) of the paraventricular anteroventral third ventricle, ligand binding increased 1.4‐fold in the paraventricular nucleus (PVN) of the hypothalamus. These findings suggest that sFR stimulates the central RAS by increasing AT(1)R expression in the PVN as a compensatory response to the reduction in basal MAP and HR. These findings have implications for people experiencing a period of sFR since an activated central RAS could increase their risk of disorders involving over activation of the RAS including renal and cardiovascular diseases. John Wiley and Sons Inc. 2020-01-10 /pmc/articles/PMC6954120/ /pubmed/31925945 http://dx.doi.org/10.14814/phy2.14338 Text en © 2020 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Research
De Souza, Aline Maria Arlindo
Linares, Andrea
Speth, Robert C.
Campos, Glenda V.
Ji, Hong
Chianca, Deoclécio
Sandberg, Kathryn
De Menezes, Rodrigo C. A.
Severe food restriction activates the central renin angiotensin system
title Severe food restriction activates the central renin angiotensin system
title_full Severe food restriction activates the central renin angiotensin system
title_fullStr Severe food restriction activates the central renin angiotensin system
title_full_unstemmed Severe food restriction activates the central renin angiotensin system
title_short Severe food restriction activates the central renin angiotensin system
title_sort severe food restriction activates the central renin angiotensin system
topic Original Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6954120/
https://www.ncbi.nlm.nih.gov/pubmed/31925945
http://dx.doi.org/10.14814/phy2.14338
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