Enhanced angiotensin II induced sodium appetite in renovascular hypertensive rats

Roncari, Camila F.; Barbosa, Rafaela Moreira; Vendramini, Regina Célia; Luca, Laurival A. De; Menani, José Vanderlei; Colombari, Eduardo

doi:10.1016/j.peptides.2017.12.025

Cited by 14 publications

(15 citation statements)

References 40 publications

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“…A number of previous studies have shown that the brain RAS is involved in stimulation of sodium intake and that actions of RAS components, especially ANG II, in the SFO and lamina terminalis (2,5,25,29,44). We recently showed that the PRR is a functional component of the brain RAS that mediates ANG II formation and regulates other RAS components (1).…”

Section: Discussionmentioning

confidence: 99%

Neuronal (pro)renin receptor regulates deoxycorticosterone-induced sodium intake

Trebak

Feng

2018

Physiological Genomics

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Increased sodium appetite is a physiological response to sodium deficiency; however, it has also been implicated in disease conditions such as congestive heart failure, kidney failure, and salt-sensitive hypertension. The central nervous system is the major regulator of sodium appetite and intake behavior; however, the neural mechanisms underlying this behavior remain incompletely understood. Here, we investigated the involvement of the (pro)renin receptor (PRR), a component of the brain renin-angiotensin system, in the regulation of sodium intake in a neuron-specific PRR knockout (PRRKO) mouse model generated previously in our laboratory. Sodium intake following deoxycorticosterone (DOCA) stimulation was tested by assessing the preference of mice for 0.9% saline or regular water in single-animal metabolic cages. Blood pressure was monitored in conscious, freely moving mice by a telemetry system. We found that saline intake and total fluid intake were significantly reduced in PRRKO mice following DOCA treatment compared with that in wild-type (WT) mice, whereas regular water intake was similar between the genotypes. Sodium preference and total sodium intake were significantly reduced in PRRKO mice compared with WT mice. PRRKO mice also excreted less urine and urinary sodium compared with WT mice following DOCA treatment, whereas potassium excretion was similar between the two groups. Finally, we found that the sodium balance, calculated by subtracting urinary sodium excretion from sodium intake, was greater in WT mice than in PRRKO mice. Collectively, these findings suggest that the neuronal PRR plays a regulatory role in DOCA-induced sodium intake.

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Section: Discussionmentioning

confidence: 99%

Neuronal (pro)renin receptor regulates deoxycorticosterone-induced sodium intake

Trebak

Feng

2018

Physiological Genomics

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“…Dietary sodium deprivation elicits a strong salt appetite in rats, 86 as does bilateral adrenalectomy, 87,88 aldosterone via its actions on the brain, 89,90 and hypovolaemic stimuli. [94][95][96][97][98] However, sodium intake is not always stimulated when hypovolaemia is present or when blood angiotensin II levels are elevated. [94][95][96][97][98] However, sodium intake is not always stimulated when hypovolaemia is present or when blood angiotensin II levels are elevated.…”

Section: Salt Appetitementioning

confidence: 99%

“…[91][92][93] The AV3V region is strongly implicated in salt appetite, in part via central angiotensin II pathways from the subfornical organ. [94][95][96][97][98] However, sodium intake is not always stimulated when hypovolaemia is present or when blood angiotensin II levels are elevated.…”

Section: Salt Appetitementioning

confidence: 99%

The osmoresponsiveness of oxytocin and vasopressin neurones: Mechanisms, allostasis and evolution

Leng

Russell

2019

J Neuroendocrinology

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In the rat supraoptic nucleus, every oxytocin cell projects to the posterior pituitary, and is involved both in reflex milk ejection during lactation and in regulating uterine contractions during parturition. All are also osmosensitive, regulating natriuresis. All are also regulated by signals that control appetite, including the neural and hormonal signals that arise from the gut after food intake and from the sites of energy storage. All are also involved in sexual behaviour, anxiety‐related behaviours and social behaviours. The challenge is to understand how a single population of neurones can coherently regulate such a diverse set of functions and adapt to changing physiological states. Their multiple functions arise from complex intrinsic properties that confer sensitivity to a wide range of internal and environmental signals. Many of these properties have a distant evolutionary origin in multifunctional, multisensory neurones of Urbilateria, the hypothesised common ancestor of vertebrates, insects and worms. Their properties allow different patterns of oxytocin release into the circulation from their axon terminals in the posterior pituitary into other brain areas from axonal projections, as well as independent release from their dendrites.

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“…Finally, Fos expression in the MnPO/OVLT located in the forebrain, in the iNTS, and in the brain stem increased in WD 2K1C rats, and further increased after 2 h of rehydration. Many studies have shown the importance of ANG II for water intake and sodium appetite (Sato et al, 1996;McKinley and Johnson, 2004;McKinley et al, 2015;Roncari et al, 2018). WD induces increased plasma osmolarity and renin levels that promote thirst and sodium appetite (Sato et al, 1996;De Luca Jr et al, 2002).…”

Section: Discussionmentioning

confidence: 99%

“…Renovascular hypertension is a type of secondary hypertension caused mainly by atherosclerotic renal artery stenosis, followed by fibromuscular disease, arteritis, thrombosis, arterial dissection, and stenosis in a transplanted kidney [reviewed in ( Derkx and Schalekamp, 1994 ; Textor, 2017 ; Herrmann and Textor, 2018 )], and account for approximately 5–6% of high blood pressure cases in the elderly ( Hansen et al, 2002 ). The increase in renin–angiotensin–aldosterone system (RAAS) activity has a pivotal role in the development of renovascular hypertension ( Leenen et al, 1975 ; Lincevicius et al, 2015 ; Textor, 2017 ; Roncari et al, 2018 ). In fact, the central or peripheral administration of AT1 receptor or aldosterone receptor antagonist was efficient in decreasing the high blood pressure levels of renovascular hypertension similar to that in 2-kidney-1clip (2K1C) rats ( Wilcox et al, 1996 ; de Oliveira-Sales et al, 2010 ; Lincevicius et al, 2015 ; Boshra and Abbas, 2017 ).…”

Section: Introductionmentioning

confidence: 99%

ANG II and Aldosterone Acting Centrally Participate in the Enhanced Sodium Intake in Water-Deprived Renovascular Hypertensive Rats

2021

Self Cite

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Renovascular hypertension is a type of secondary hypertension caused by renal artery stenosis, leading to an increase in the renin–angiotensin–aldosterone system (RAAS). Two-kidney, 1-clip (2K1C) is a model of renovascular hypertension in which rats have an increased sodium intake induced by water deprivation (WD), a common situation found in the nature. In addition, a high-sodium diet in 2K1C rats induces glomerular lesion. Therefore, the purpose of this study was to investigate whether angiotensin II (ANG II) and/or aldosterone participates in the increased sodium intake in 2K1C rats under WD. In addition, we also verified if central AT1 and mineralocorticoid receptor blockade would change the high levels of arterial pressure in water-replete (WR) and WD 2K1C rats, because blood pressure changes can facilitate or inhibit water and sodium intake. Finally, possible central areas activated during WD or WD followed by partial rehydration (PR) in 2K1C rats were also investigated. Male Holtzman rats (150–180 g) received a silver clip around the left renal artery to induce renovascular hypertension. Six weeks after renal surgery, a stainless-steel cannula was implanted in the lateral ventricle, followed by 5–7 days of recovery before starting tests. Losartan (AT1 receptor antagonist) injected intracerebroventricularly attenuated water intake during the thirst test. Either icv losartan or RU28318 (mineralocorticoid receptor antagonist) reduced 0.3 M NaCl intake, whereas the combination of losartan and RU28318 icv totally blocked 0.3 M NaCl intake induced by WD in 2K1C rats. Losartan and RU28318 icv did not change hypertension levels of normohydrated 2K1C rats, but reduced the increase in mean arterial pressure (MAP) produced by WD. c-Fos expression increased in the lamina terminalis and in the NTS in WD condition, and increased even more after WD-PR. These results suggest the participation of ANG II and aldosterone acting centrally in the enhanced sodium intake in WD 2K1C rats, and not in the maintenance of hypertension in satiated and fluid-replete 2K1C rats.

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Enhanced angiotensin II induced sodium appetite in renovascular hypertensive rats

Cited by 14 publications

References 40 publications

Neuronal (pro)renin receptor regulates deoxycorticosterone-induced sodium intake

Neuronal (pro)renin receptor regulates deoxycorticosterone-induced sodium intake

The osmoresponsiveness of oxytocin and vasopressin neurones: Mechanisms, allostasis and evolution

ANG II and Aldosterone Acting Centrally Participate in the Enhanced Sodium Intake in Water-Deprived Renovascular Hypertensive Rats

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