Distribution of Fos immunoreactivity in rat brain after sodium consumption induced by peritoneal dialysis

1999 ◽  
Vol 276 (4) ◽  
pp. R1180-R1187 ◽  
Author(s):  
Lucia F. Franchini ◽  
Laura Vivas
Keyword(s):  
Peritoneal Dialysis ◽  
Area Postrema ◽  
Neuronal Population ◽  
Sodium Balance ◽  
Sodium Appetite ◽  
Lateral Parabrachial Nucleus ◽  
Sodium Ingestion ◽  
Oxytocinergic Neurons ◽  
Neuronal Groups ◽  
Sodium Consumption

Fos immunoreactivity was used to map the neuronal population groups activated after sodium ingestion induced by peritoneal dialysis (PD) in rats. Oxytocin immunoreactivity in combination with Fos immunoreactivity was also analyzed to evaluate whether the oxytocinergic neurons of the paraventricular nucleus of the hypothalamus (PVN) are activated during the satiety process of sodium appetite. Sodium ingestion stimulated by PD produced Fos immunoreactivity within defined cells groups of the lamina terminalis and hindbrain areas such us the nucleus of the solitary tract, area postrema, and lateral parabrachial nucleus. On the other hand, particular parvocellular and magnocellular oxytocinergic subdivisions of the PVN and supraoptic nucleus were double labeled after PD-induced sodium consumption. Approximately 27 and 2.1%, respectively, of the activated dorsomedial cap and parvocellular posterior subnuclei of the PVN, which project to the hindbrain, were oxytocinergic. Our data indicate that specific neuronal groups are activated during the satiety process of sodium appetite, suggesting they may form a circuit subserving sodium balance regulation. They also support a functional role for the oxytocinergic neurons in this circuit.

Sodium appetite and Fos activation in serotonergic neurons

2002 ◽  
Vol 282 (1) ◽  
pp. R235-R243 ◽  
Author(s):  
Lucia F. Franchini ◽  
Alan Kim Johnson ◽  
José de Olmos ◽  
Laura Vivas
Keyword(s):  
Peritoneal Dialysis ◽  
Area Postrema ◽  
Sodium Balance ◽  
Not Given ◽  
Nacl Solution ◽  
Sodium Depletion ◽  
Serotonergic Neurons ◽  
Sodium Appetite ◽  
Sodium Ingestion ◽  
Solution Intake

We evaluated serotonergic hindbrain groups of cells for their involvement in the generation and inhibition of sodium appetite. For that purpose, we analyzed the number of Fos-immunoreactive (Fos-ir) cells and double-labeled Fos-serotonin (5-HT)-ir neurons within different nuclei of the hindbrain raphe system and the area postrema (AP). Sodium depletion and sodium appetite were induced by peritoneal dialysis. Twenty-four hours after peritoneal dialysis, a 2% NaCl solution intake test was given to peritoneal dialyzed animals [PD-with access (PD-A) group] and to control dialyzed animals [CD-with access (CD-A) group]. Two additional groups of animals received either peritoneal dialysis or control dialysis but were not given access to the 2% NaCl [CD-no access (CD-NA) group or PD-no access (PD-NA) group]. The number of Fos-ir neurons within different nuclei of the raphe system was increased in spontaneous and induced sodium ingestion of CD-A and PD-A groups compared with the CD-NA and PD-NA groups. The PD-NA group had significantly fewer double-labeled cells along the raphe system compared with the animals in near-normal sodium balance (CD-NA and CD-A) or in the process of restoring sodium balance by consuming NaCl (PD-A). The AP of the PD-A group showed a significant increase in the number of Fos-ir and Fos-5-HT-ir cells compared with the PD-NA and CD groups. Our results suggest that serotonergic pathways with cell bodies in the AP and the raphe system are involved in the control of sodium appetite.

Water deprivation-induced sodium appetite and differential expression of encephalic c-Fos immunoreactivity in the spontaneously hypertensive rat

2010 ◽  
Vol 298 (5) ◽  
pp. R1298-R1309 ◽  
Author(s):  
Daniela T. B. Pereira-Derderian ◽  
Regina C. Vendramini ◽  
José V. Menani ◽  
Laurival A. De Luca
Keyword(s):  
Water Intake ◽  
Water Deprivation ◽  
Spontaneously Hypertensive Rat ◽  
Area Postrema ◽  
Cell Activity ◽  
Sodium Balance ◽  
Lamina Terminalis ◽  
Spontaneously Hypertensive ◽  
Sodium Appetite ◽  
Hypertensive Rat

The spontaneously hypertensive rat (SHR) has an intense consumption of NaCl solution. Water deprivation (WD) followed by water intake to satiety induces partial rehydration (PR)—the WD-PR protocol—and sodium appetite. In the present work, WD produced similar water intake and no alterations in arterial pressure among spontaneously hypertensive rat (SHR), Wistar-Kyoto, and Holtzman strains. It also increased the number of cells with positive c-Fos immunoreactivity (Fos-IR) in the lamina terminalis and in the hypothalamic supraoptic (SON) and paraventricular (parvocellular, PVNp) nucleus in these strains. The WD and WD-PR produced similar alterations in all strains in serum osmolality and protein, plasma renin activity, and sodium balance. The SHR ingested about 10 times more 0.3 M NaCl than normotensives strains in the sodium appetite test that follows WD-PR. After WD-PR, the Fos-IR persisted, elevated in the lamina terminalis of all strains but notably in the subfornical organ of the SHR. The WD-PR reversed Fos-IR in the SON of all strains and in the PVNp of SHR. It induced Fos-IR in the area postrema and in the nucleus of the solitary tract (NTS), dorsal raphe, parabrachial (PBN), pre-locus coeruleus (pre-LC), suprachiasmatic, and central amygdalar nucleus of all strains. This effect was bigger in the caudal-NTS, pre-LC, and medial-PBN of SHRs. The results indicate that WD-PR increases cell activity in the forebrain and hindbrain areas that control sodium appetite in the rat. They also suggest that increased cell activity in facilitatory brain areas precedes the intense 0.3 M NaCl intake of the SHR in the sodium appetite test.

Rapid-onset "need-free" sodium appetite after lesions of the dorsomedial medulla

1993 ◽  
Vol 264 (6) ◽  
pp. R1242-R1247 ◽  
Author(s):  
G. L. Edwards ◽  
T. G. Beltz ◽  
J. D. Power ◽  
A. K. Johnson
Keyword(s):  
Area Postrema ◽  
Extracellular Fluid ◽  
Rapid Onset ◽  
Sodium Balance ◽  
Bilateral Nephrectomy ◽  
Sodium Appetite ◽  
Fluid Compartment ◽  
Sodium Loss ◽  
Ad Libitum Intake ◽  
Saline Solutions

Previous studies indicate the dorsomedial hindbrain is important in the maintenance of fluid balance. Lesions centering on the area postrema (AP) result in enhanced ad libitum intake of concentrated saline solutions on a 24-h basis as well as enhanced excretion of water and electrolytes. Additionally, rats with lesions of the AP are reported to have an exaggerated behavioral response to dipsogenic challenges that mimic depletion of the extracellular fluid compartment. In the studies reported here, we have observed that rats with lesions of the AP and immediately adjacent nucleus of the solitary tract consume large quantities of concentrated saline solutions within minutes of presentation. This intake does not appear to be related to sodium loss or depletion because the lesioned rats are in a positive sodium balance and the appetite persists after bilateral nephrectomy. These data, in conjunction with earlier studies, suggest that the dorsomedial medulla, including the AP, acts to prevent overconsumption of water and sodium that could result in increased extracellular fluid volume.

scholarly journals Effect of sex chromosome complement on sodium appetite and Fos-immunoreactivity induced by sodium depletion

2014 ◽  
Vol 306 (3) ◽  
pp. R175-R184 ◽  
Author(s):  
Florencia M. Dadam ◽  
Ximena E. Caeiro ◽  
Carla D. Cisternas ◽  
Ana F. Macchione ◽  
María J. Cambiasso ◽  
...  
Keyword(s):  
Sex Chromosome ◽  
Area Postrema ◽  
Brain Activity ◽  
Chromosome Complement ◽  
Circumventricular Organs ◽  
Sexually Dimorphic ◽  
Sodium Depletion ◽  
Sodium Diet ◽  
Sodium Appetite ◽  
Low Sodium Diet

Previous studies indicate a sex chromosome complement (SCC) effect on the angiotensin II-sexually dimorphic hypertensive and bradycardic baroreflex responses. We sought to evaluate whether SCC may differentially modulate sexually dimorphic-induced sodium appetite and specific brain activity due to physiological stimulation of the rennin angiotensin system. For this purpose, we used the “four core genotype” mouse model, in which the effect of gonadal sex and SCC is dissociated, allowing comparisons of sexually dimorphic traits between XX and XY females as well as in XX and XY males. Gonadectomized mice were sodium depleted by furosemide (50 mg/kg) and low-sodium diet treatment; control groups were administered with vehicle and maintained on normal sodium diet. Twenty-one hours later, the mice were divided into two groups: one group was submitted to the water-2% NaCl choice intake test, while the other group was perfused and their brains subjected to the Fos-immunoreactivity (FOS-ir) procedure. Sodium depletion, regardless of SCC (XX or XY), induced a significantly lower sodium and water intake in females than in males, confirming the existence in mice of sexual dimorphism in sodium appetite and the organizational involvement of gonadal steroids. Moreover, our results demonstrate a SCC effect on induced brain FOS-ir, showing increased brain activity in XX-SCC mice at the paraventricular nucleus, nucleus of the solitary tract, and lateral parabrachial nucleus, as well as an XX-SCC augmented effect on sodium depletion-induced brain activity at two circumventricular organs, the subfornical organ and area postrema, nuclei closely involved in fluid and blood pressure homeostasis.

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

2018 ◽  
Vol 50 (10) ◽  
pp. 904-912 ◽  
Author(s):  
Fatima Trebak ◽  
Wencheng Li ◽  
Yumei Feng
Keyword(s):  
Sodium Intake ◽  
Renin Angiotensin System ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Balance ◽  
Total Fluid Intake ◽  
Sodium Deficiency ◽  
Sodium Appetite ◽  
The Central Nervous System ◽  
Salt Sensitive Hypertension

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.

Amiloride-sensitive sodium channels and expression of sodium appetite in rats

1987 ◽  
Vol 253 (2) ◽  
pp. R371-R374 ◽  
Author(s):  
I. L. Bernstein ◽  
C. J. Hennessy
Keyword(s):  
Sodium Channels ◽  
Transport System ◽  
Sodium Transport ◽  
Taste Bud ◽  
Sodium Balance ◽  
Gustatory System ◽  
Sodium Appetite ◽  
Amiloride Hydrochloride

Lingual application of amiloride hydrochloride blocks a sodium transport system in the mammalian gustatory system. Effects of exposure to amiloride on subsequent licking for 3% NaCl by rats were found to differ as a function of the animal's sodium balance. Licking for 3% NaCl was significantly increased in sodium-replete rats and significantly decreased in sodium-deplete rats by amiloride pretreatment. In fact, expression of sodium appetite was virtually eliminated by pretreatment with amiloride. This suggests that the recognition of sodium solutions in animals with a sodium deficit is dependent on amiloride-sensitive sodium transport at the taste bud.

Sodium, Potassium and Nitrogen Balances in Chronic Nephrectomized Dogs

1956 ◽  
Vol 185 (1) ◽  
pp. 175-178
Author(s):  
C. Riley Houck
Keyword(s):  
Peritoneal Dialysis ◽  
Plasma Protein ◽  
Nitrogen Balance ◽  
Potassium Concentration ◽  
The Body ◽  
Sodium Balance ◽  
Sodium Potassium ◽  
Peritoneal Dialysate ◽  
Low Salt

Twelve bilaterally nephrectomized dogs on a low-salt, 54 cal/kg/day diet were maintained for periods up to 3 weeks by intermittent peritoneal dialysis. This procedure maintained the animals in normal sodium balance but provided both a negative potassium and nitrogen balance. The over-all loss of potassium occurred even though the dialysate potassium concentration was varied from 2.8–3.7 mEq/l. It is believed that the negative K and N balances are brought about by loss of plasma protein and some erythrocytes into the peritoneal dialysate. The data indicate that K and N are not lost from the body in the same ratio that they occur in tissues. Renoprival hypertension developes despite failure of the body to retain sodium and despite loss of both potassium and nitrogen from the body.

Renin and aldosterone secretions during hypovolemia in rats: relation to NaCl intake

1979 ◽  
Vol 237 (1) ◽  
pp. R45-R51 ◽  
Author(s):  
E. M. Stricker ◽  
A. H. Vagnucci ◽  
R. H. McDonald ◽  
F. H. Leenen
Keyword(s):  
Sodium Intake ◽  
Plasma Renin ◽  
The Other ◽  
Bilateral Nephrectomy ◽  
Deficient Diet ◽  
Sodium Appetite ◽  
Wide Range ◽  
Peg Treatment ◽  
Sodium Consumption ◽  
Clear Relation

Plasma renin activities (PRA) and aldosterone concentrations increased in parallel over a wide range of plasma volume deficits produced in unanesthetized rats by extravascular administration of polyethylene glycol (PEG) solution. When PEG-treated rats were given water to drink, their intakes were proportional to PRA; when given water and 0.5 M NaCl, PRA and the steroid concentrations diminished concurrently in association with sodium consumption. Aldosterone concentrations and NaCl intakes were markedly enhanced after PEG treatment in rats maintained on a sodium-deficient diet for 4 days. On the other hand, a clear relation between PRA and water intake, and between circulating aldosterone levels and sodium intake, was not suggested by other experiments in this series. For example, bilateral nephrectomy abolished the rise in PRA during hypovolemia yet rats drank water normally. Moreover, aldosterone concentrations were substantially elevated by PEG treatment in the nephrectomized rats yet sodium appetite was abolished. These and other findings suggest that neither angiotensin nor aldosterone plays a prominent role in stimulating water and saline intakes during hypovolemia.

Hormonal and Neural Mechanisms of Sodium Appetite

Physiology ◽  
1986 ◽  
Vol 1 (2) ◽  
pp. 51-54 ◽  
Author(s):  
MJ Fregly ◽  
NE Rowland
Keyword(s):  
Sodium Content ◽  
Neural Mechanisms ◽  
Sodium Balance ◽  
Salt Appetite ◽  
Sodium Appetite ◽  
Complex Mechanisms

A strong appetite for salt seems to be a normal link in the complex mechanisms that serve to maintain a normal sodium content of the organism. Experiments with rats have helped to unravel many aspects of the endocrine mechanisms that are involved in regulating sodium balance and salt appetite, but more work is needed to understand the mechanisms that induce salt appetite in different species.

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