Sodium appetite elicited by intracerebroventricular infusion of angiotensin II in the rat: I. Relation to urinary sodium excretion.

Fluharty, Steven J.; Manaker, Scott

doi:10.1037/0735-7044.97.5.738

Cited by 51 publications

(41 citation statements)

References 10 publications

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“…These effects were described by many researchers (Fluharty and Manaker, 1983;Unger et al, 1989;Weekley, 1992;Fitzsimons, 1998;Ferguson et al, 2001;Geerling and Loewy, 2008). In addition, in the present work it was found that ANG II i.c.v.…”

Section: Resultssupporting

confidence: 77%

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A previous history of repeated amphetamine exposure modifies brain angiotensin II AT1 receptor functionality

et al. 2015

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Section: Resultssupporting

confidence: 77%

“…Furthermore, studies in mammals have demonstrated that i.c.v. ANG II administration enhanced renal sodium excretion, water and sodium intake (Fluharty and Manaker, 1983;Unger et al, 1989;Ferguson et al, 2001), increased vasopressin and oxytocin secretion and decreased plasma renin activity (Weekley, 1992;Ferguson et al, 2001).…”

Section: Introductionmentioning

confidence: 99%

A previous history of repeated amphetamine exposure modifies brain angiotensin II AT1 receptor functionality

et al. 2015

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“…While circulating AngII tends to retain sodium by a direct renal action, 9 as well as through aldosterone release from the adrenal gland, stimulation of brain AngII receptors has been reported to induce natriuresis. 10 In 1983, Fluharty and Manaker [19] demonstrate that i.c.v. infusion of AngII elicits a small, early phase of sodium appetite that is not the result of prior sodium loss, but that thereafter urinary excretion of sodium exceeds intake and consequently the animals become hyponatraemic and hypovolaemic.…”

Section: Discussionmentioning

confidence: 99%

Impaired dipsogenic and renal response to repetitive intracerebroventricular angiotensin II (AngII) injections in rats

Zapparoli

Figueiredo

Bôer

et al. 2011

J Renin Angiotensin Aldosterone Syst

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The role of the central nervous system (CNS) in the control of blood pressure and hydrosaline homeostasis has been demonstrated by several studies. While circulating angiotensin II (AngII) tends to retain sodium by a direct renal action as well as through aldosterone release, stimulation of brain AngII receptors has been reported to induce natriuresis. Repetitive intracerebroventricular AngII injection was recently demonstrated to be capable of leading to desensitisation of the dipsogenic effect of AngII stimuli. The aim of the current study was to investigate a possible central desensitisation to AngII stimuli by observing the effects of a low-concentration solution of AngII on the dipsogenic and natriuretic mechanisms in conscious rats, compared with appropriate age-matched 0.15 M NaCl-injected subjects, as evaluated by lithium clearance. The present report confirmed earlier reports on the potent natriuretic and dipsogenic effects of central AngII receptor stimulation. Natriuresis is mediated by a decrease in sodium reabsorption in the proximal and post-proximal tubule segments of the nephron. The current findings lend further support to the idea that AngII, in the CNS, is instrumental in the regulation of body fluid homeostasis. The magnitude of the dipsogenic and renal response to AngII was significantly decreased by repetitive stimulus.

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“…There is a good amount of evidence in the literature that manipulation of ANGII levels alters thirst in rats that are hydrated [8, 9]demonstrating that ANGII is directly involved in eliciting dipsogenic behavior. Some evidence also exists on the role that ANGII plays in the induction of salt appetite [4, 10, 11], although the onset of salt appetite after application of ANGII occurs much later than that of thirst [51]. It is clear nevertheless that administered ANGII promotes a series of physiological and behavioral responses whereby water and sodium are retained or released, and water and salt is ingested, respectively.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Mesolimbic Structures in Short-Term Sodium Depletion: In situ Hybridization and Ligand-Binding Analyses

Lucas

Grillo

McEwen³

2003

Neuroendocrinology

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Acute treatment with the diuretic furosemide (Lasix) produces a reduction in plasma Na⁺ and volume as well as increased thirst and salt appetite. The resulting hypovolemia stimulates the well-known counter-regulatory physiological response from the renin-angiotensin-aldosterone system. However, the neurochemical players underpinning the behavioral responses of thirst and salt appetite are less clear. Previously, we have reported that salt-replete deoxycorticosterone (DOCA) treatment activates mesolimbic structures associated with reward and goal-seeking behavior. The present study was designed to test whether the same brain regions are affected in a salt-depleted state. In experiment 1, two groups of adult male Sprague-Dawley (SD) rats were injected with Lasix (10 mg/rat, s.c.) and 18 h later were allowed access either to 2% NaCl solution (‘Lasix+salt’) or only to tap water (‘Lasixnosalt’) for 2 h. For comparison purposes, a third group received an isotonic saline injection instead of Lasix and was allowed access to the 2% salt solution (Vehicle). All groups were permitted 24 h access to tap water. We found no differences in dynorphin-mRNA levels in any striatal and accumbal regions among any of the treatment groups. However, as found previously in DOCA-treated rats, there were increased enkephalin (ENK)-mRNA and decreased dopamine transporter (DAT) binding levels throughout the striatum in Lasix+salt and decreased ENK-mRNA in Lasixnosalt rats versus Vehicle. In experiment 2, the involvement of the ENKergic and/or dopaminergic system was tested in rats divided into the same three groups described in experiment 1. However, before access to salt or water, the Lasix+salt and the vehicle groups were administered either a δ-opioid, naltrindole or a dopamine D₂ antagonist, raclopride. Only the naltrindole-treated rats showed a blunted intake of salt solution. Thus, these findings along with our neurochemical results suggest that mesolimbic enkephalin might impact salt intake through dopaminergic systems.

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Sodium appetite elicited by intracerebroventricular infusion of angiotensin II in the rat: I. Relation to urinary sodium excretion.

Cited by 51 publications

References 10 publications

A previous history of repeated amphetamine exposure modifies brain angiotensin II AT1 receptor functionality

A previous history of repeated amphetamine exposure modifies brain angiotensin II AT1 receptor functionality

Impaired dipsogenic and renal response to repetitive intracerebroventricular angiotensin II (AngII) injections in rats

Involvement of Mesolimbic Structures in Short-Term Sodium Depletion: In situ Hybridization and Ligand-Binding Analyses

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