Open AccessSevere food restriction activates the central renin angiotensin system
Author(s) -
De Souza Aline Maria Arlindo,
Linares Andrea,
Speth Robert C.,
Campos Glenda V.,
Ji Hong,
Chianca Deoclécio,
Sandberg Kathryn,
De Menezes Rodrigo C. A.
Publication year - 2020
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.14338
Subject(s) - subfornical organ , median preoptic nucleus , medicine , endocrinology , microinjection , renin–angiotensin system , hypothalamus , angiotensin ii , losartan , lamina terminalis , preoptic area , third ventricle , circumventricular organs , basal (medicine) , blood pressure , insulin
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.