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|Title:||Role of the renin angiotensin system in blood pressure allostasis-induced by severe food restriction in female Fischer rats.|
|Authors:||Souza, Aline Maria Arlindo de|
West, Crystal A.
Abreu, Aline Rezende Ribeiro de
Pai, Amrita V.
Mesquita, Laura Batista Tavares
Chianca Júnior, Deoclécio Alves
Menezes, Rodrigo Cunha Alvim de
|Citation:||SOUZA , A. M. A. de et. Role of the renin angiotensin system in blood pressure allostasis-induced by severe food restriction in female Fischer rats. Scientific Reports, v. 8, p. 1-15, 2018. Disponível em: <https://www.nature.com/articles/s41598-018-28593-6>. Acesso em: 22 fev. 2019.|
|Abstract:||Severe food restriction (FR) is associated with blood pressure (BP) and cardiovascular dysfunction. The renin-angiotensin system (RAS) regulates BP and its dysregulation contributes to impaired cardiovascular function. Female Fischer rats were maintained on a control (CT) or severe FR (40% of CT) diet for 14 days. In response to severe FR, BP allostasis was achieved by up-regulating circulating Ang-[1–8] by 1.3-fold through increased angiotensin converting enzyme (ACE) activity and by increasing the expression of AT1Rs 1.7-fold in mesenteric vessels. Activation of the RAS countered the depressor effect of the severe plasma volume reduction (≥30%). The RAS, however, still underperformed as evidenced by reduced pressor responses to Ang-[1–8] even though AT1Rs were still responsive to the depressor effects of an AT1R antagonist. The aldosterone (ALDO) response was also inadequate as no changes in plasma ALDO were observed after the large fall in plasma volume. These findings have implications for individuals who have experienced a period(s) of severe FR (e.g., anorexia nervosa, dieters, natural disasters) and suggests increased activity of the RAS in order to achieve allostasis contributes to the cardiovascular dysfunction associated with inadequate food intake.|
|metadata.dc.rights.license:||This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. Fonte: o próprio artigo|
|Appears in Collections:||DECBI - Artigos publicados em periódicos|
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