Please use this identifier to cite or link to this item: http://www.repositorio.ufop.br/jspui/handle/123456789/13978
Title: Severe food restriction activates the central renin angiotensin system.
Authors: Souza, Aline Maria Arlindo de
Linares, Andrea
Speth, Robert
Campos, Glenda Siqueira Viggiano
Ji, Hong
Chianca Júnior, Deoclécio Alves
Sandberg, Kathryn
Menezes, Rodrigo Cunha Alvim de
Keywords: Angiotensin converting enzyme (ACE)
Angiotensin converting enzyme 2 (ACE2)
Caloric reduction
Inadequate food intake
RAS-Fingerprint
Issue Date: 2020
Citation: SOUZA, A. M. A. de et al. Severe food restriction activates the central renin angiotensin system. Physiological Reports, v. 8, p. 1-12, 2020. Disponível em: <https://physoc.onlinelibrary.wiley.com/doi/full/10.14814/phy2.14338>. Acesso em: 10 jun. 2021.
Abstract: 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 AT1R 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 AT1R 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.
URI: http://www.repositorio.ufop.br/jspui/handle/123456789/13978
metadata.dc.identifier.doi: https://doi.org/10.14814/phy2.14338
ISSN: 2051-817X
metadata.dc.rights.license: 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. Source: The article PDF.
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