Angiotensin and salt appetite of BALB/c mice

1990 ◽  
Vol 259 (4) ◽  
pp. R729-R735 ◽  
Author(s):  
D. A. Denton ◽  
J. R. Blair-West ◽  
M. McBurnie ◽  
P. G. Osborne ◽  
E. Tarjan ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Sodium Content ◽  
Neural Systems ◽  
Salt Appetite ◽  
Nacl Solution ◽  
Sodium Appetite ◽  
Daily Water Intake ◽  
Body Sodium ◽  
Daily Water ◽  
Ingestive Behaviors

The influence of systemic or intracerebroventricular (icv) administration of angiotensin II on the intakes of NaCl solution, water, and food was investigated in BALB/c mice. Systemic administration of angiotensin II had little, if any, influence on these ingestive behaviors. On the other hand, icv infusion of angiotensin II at 70 ng/day increased (P less than 0.05) intakes of NaCl solution and water by the third day of infusion. The amount of NaCl ingested daily during the infusion was two to three times body sodium content. The mean daily water intake increased to 40-60% of body weight. The vast increase in NaCl intake was not secondary to a natriuresis caused by the icv infusion of angiotensin II. The results suggest that angiotensin II has a direct effect on neural systems involved in sodium appetite in this species.

Ingestive responses to administration of stress hormones in baboons

2002 ◽  
Vol 282 (1) ◽  
pp. R10-R18 ◽  
Author(s):  
R. E. Shade ◽  
J. R. Blair-West ◽  
K. D. Carey ◽  
L. J. Madden ◽  
R. S. Weisinger ◽  
...  
Keyword(s):  
Stress Hormones ◽  
Stress Hormone ◽  
Nacl Solution ◽  
Sodium Appetite ◽  
Arterial Blood ◽  
Daily Food ◽  
Daily Water Intake ◽  
Daily Water ◽  
Voluntary Intake ◽  
Ingestive Behaviors

Experimental stress and the administration of the stress hormone ACTH have been reported to stimulate sodium appetite in many nonprimate species. Experiments were conducted to determine whether prolonged intracerebroventricular infusions of the neuropeptides corticotropin-releasing factor (CRF) and urocortin (Ucn), or systemic administration of ACTH, affected ingestive behaviors in a nonhuman primate, the baboon. Intracerebroventricular infusions of CRF or Ucn significantly decreased daily food intake. The decrease with Ucn continued into the postinfusion period. These infusions did not alter daily water intake. Daily voluntary intake of 300 mM NaCl solution was not increased, and there was evidence of reductions on days 2- 4 of the infusions. Intramuscular injections of porcine ACTH or synthetic ACTH (Synacthen) for 5 days did not affect daily NaCl intake, although the doses were sufficient to increase cortisol secretion and arterial blood pressure. Sodium depletion by 3 days of furosemide injections did induce a characteristic sodium appetite in the same baboons. These results demonstrate the anorexigenic action of CRF and Ucn in this primate. Also, CRF, Ucn, and ACTH did not stimulate sodium appetite at the doses used.

Angiotensin II-induced thirst, but not sodium appetite, via AT1 receptors in organum cavum prelamina terminalis

1995 ◽  
Vol 268 (6) ◽  
pp. R1401-R1405 ◽  
Author(s):  
M. el Ghissassi ◽  
S. N. Thornton ◽  
S. Nicolaidis
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
High Sensitivity ◽  
Ang Ii ◽  
Nacl Solution ◽  
At1 Receptors ◽  
Sodium Appetite ◽  
Specific Antagonist

The angiotensin receptor specificity, with respect to fluid intake, of the organum cavum prelamina terminalis (OCPLT), a recently discovered discrete forebrain structure with high sensitivity to angiotensin II (ANG II), was investigated. ANG II (10 ng) microinjected into the OCPLT significantly increased water consumption but did not induce intake of a hypertonic (3%) NaCl solution. Losartan, an ANG II type 1 (AT1) receptor-specific antagonist, produced dose-related (1-100 ng) inhibition of ANG II-induced drinking. The ANG II type 2 receptor-specific antagonist CGP-42112A was ineffective. Intake of the 3% NaCl solution in response to microinjection of either of the antagonists into the OCPLT was never observed. These findings suggest that water intake produced by microinjection of ANG II into the OCPLT is mediated by AT1 receptors uniquely and that, in contrast to other regions of the brain, these receptors do not induce salt intake when stimulated by ANG II.

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.

scholarly journals Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

2007 ◽  
Vol 293 (3) ◽  
pp. R1027-R1036 ◽  
Author(s):  
Andrea Godino ◽  
Laurival Antonio De Luca ◽  
José Antunes-Rodrigues ◽  
Laura Vivas
Keyword(s):  
Plasma Levels ◽  
Supraoptic Nucleus ◽  
Sodium Intake ◽  
The Body ◽  
Nacl Solution ◽  
Sodium Appetite ◽  
Body Sodium ◽  
Intake Regulation ◽  
Sodium Consumption ◽  
Sodium Solution

Previous studies demonstrated the inhibitory participation of serotonergic (5-HT) and oxytocinergic (OT) neurons on sodium appetite induced by peritoneal dialysis (PD) in rats. The activity of 5-HT neurons increases after PD-induced 2% NaCl intake and decreases after sodium depletion; however, the activity of the OT neurons appears only after PD-induced 2% NaCl intake. To discriminate whether the differential activations of the 5-HT and OT neurons in this model are a consequence of the sodium satiation process or are the result of stimulation caused by the entry to the body of a hypertonic sodium solution during sodium access, we analyzed the number of Fos-5-HT- and Fos-OT-immunoreactive neurons in the dorsal raphe nucleus and the paraventricular nucleus of the hypothalamus-supraoptic nucleus, respectively, after isotonic vs. hypertonic NaCl intake induced by PD. We also studied the OT plasma levels after PD-induced isotonic or hypertonic NaCl intake. Sodium intake induced by PD significantly increased the number of Fos-5-HT cells, independently of the concentration of NaCl consumed. In contrast, the number of Fos-OT neurons increased after hypertonic NaCl intake, in both depleted and nondepleted animals. The OT plasma levels significantly increased only in the PD-induced 2% NaCl intake group in relation to others, showing a synergic effect of both factors. In summary, 5-HT neurons were activated after body sodium status was reestablished, suggesting that this system is activated under conditions of satiety. In terms of the OT system, both OT neural activity and OT plasma levels were increased by the entry of hypertonic NaCl solution during sodium consumption, suggesting that this system is involved in the processing of hyperosmotic signals.

Mice deficient in oxytocin manifest increased saline consumption following overnight fluid deprivation

2001 ◽  
Vol 281 (5) ◽  
pp. R1368-R1373 ◽  
Author(s):  
Janet A. Amico ◽  
Mariana Morris ◽  
Regis R. Vollmer
Keyword(s):  
Tap Water ◽  
Daily Intake ◽  
Choice Test ◽  
Salt Appetite ◽  
Nacl Solution ◽  
Total Water ◽  
Sodium Appetite ◽  
Significant Difference ◽  
Deficient Mice ◽  
Observation Period

Male mice (9–13 mo of age) in which the gene for oxytocin (OT) had been deleted (OT −/−) were administered 0.5 M sodium chloride (NaCl) solution or tap water as a two-bottle choice test following overnight fluid deprivation (1600 to 1000 the following day). Compared with wild-type cohorts (OT +/+), OT-deficient mice ingested sevenfold greater amounts of saline in the first hour following reintroduction of fluids, P < 0.001, and fourfold greater amounts at the end of 6 h, P < 0.02. No significant difference in total water ingested was noted between the two genotypes at the end of either 1 or 6 h. If food deprivation accompanied the overnight fluid deprivation and food was reintroduced 1 h after the reintroduction of both water and saline, OT −/− mice still ingested greater amounts of saline, but not water, than OT +/+ mice at both 1 h, P < 0.001, and 6 h, P< 0.02. No differences were noted between genotypes in the daily intake of 0.5 M NaCl solution or water during a 3-day observation period before the overnight fluid deprivation. The volume of saline consumed in each 24-h observation period represented about one-tenth of the total fluids ingested in each genotype. We conclude that OT −/− mice display an enhanced salt appetite compared with OT +/+ mice when fluid deprived overnight. The salt appetite was only apparent in the presence of a perturbation such as fluid deprivation, which predisposes the animal to moderate hypovolemia. The observations support an inhibitory role for OT in the control of sodium appetite in mice.

scholarly journals Sodium Imbalance in Mice Results Primarily in Compensatory Gene Regulatory Responses in Kidney and Colon, but Not in Taste Tissue

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 995 ◽  
Author(s):  
Kristina Lossow ◽  
Wolfgang Meyerhof ◽  
Maik Behrens
Keyword(s):  
Prolonged Exposure ◽  
Bitter Taste ◽  
Sodium Content ◽  
Dietary Sodium ◽  
Salt Appetite ◽  
Dietary Salt ◽  
Sodium Homeostasis ◽  
Salt Taste ◽  
Sodium Appetite

Renal excretion and sodium appetite provide the basis for sodium homeostasis. In both the kidney and tongue, the epithelial sodium channel (ENaC) is involved in sodium uptake and sensing. The diuretic drug amiloride is known to block ENaC, producing a mild natriuresis. However, amiloride is further reported to induce salt appetite in rodents after prolonged exposure as well as bitter taste impressions in humans. To examine how dietary sodium content and amiloride impact on sodium appetite, mice were subjected to dietary salt and amiloride intervention and subsequently analyzed for ENaC expression and taste reactivity. We observed substantial changes of ENaC expression in the colon and kidney confirming the role of these tissues for sodium homeostasis, whereas effects on lingual ENaC expression and taste preferences were negligible. In comparison, prolonged exposure to amiloride-containing drinking water affected β- and αENaC expression in fungiform and posterior taste papillae, respectively, next to changes in salt taste. However, amiloride did not only change salt taste sensation but also perception of sucrose, glutamate, and citric acid, which might be explained by the fact that amiloride itself activates bitter taste receptors in mice. Accordingly, exposure to amiloride generally affects taste impression and should be evaluated with care.

Osmoregulatory fluid intake but not hypovolemic thirst is intact in mice lacking angiotensin

2008 ◽  
Vol 294 (5) ◽  
pp. R1533-R1543 ◽  
Author(s):  
Michael J. McKinley ◽  
Lesley L. Walker ◽  
Theodora Alexiou ◽  
Andrew M. Allen ◽  
Duncan J. Campbell ◽  
...  
Keyword(s):  
Polyethylene Glycol ◽  
Angiotensin Ii ◽  
Water Intake ◽  
Subfornical Organ ◽  
Salt Appetite ◽  
Neural Pathways ◽  
Daily Water Intake ◽  
Similar Dose ◽  
Central Origin ◽  
Supraoptic Nuclei

Water intakes in response to hypertonic, hypovolemic, and dehydrational stimuli were investigated in mice lacking angiotensin II as a result of deletion of the angiotensinogen gene (Agt−/− mice), and in C57BL6 wild-type (WT) mice. Baseline daily water intake in Agt−/− mice was approximately threefold that of WT mice because of a renal developmental disorder of the urinary concentrating mechanisms in Agt−/− mice. Intraperitoneal injection of hypertonic saline (0.4 and 0.8 mol/l NaCl) caused a similar dose-dependent increase in water intake in both Agt−/− and WT mice during the hour following injection. As well, Agt−/− mice drank appropriate volumes of water following water deprivation for 7 h. However, Agt−/− mice did not increase water or 0.3 mol/l NaCl intake in the 8 h following administration of a hypovolemic stimulus (30% polyethylene glycol sc), whereas WT mice increased intakes of both solutions during this time. Osmoregulatory regions of the brain [hypothalamic paraventricular and supraoptic nuclei, median preoptic nucleus, organum vasculosum of the lamina terminalis (OVLT), and subfornical organ] showed an increased number of neurons exhibiting Fos-immunoreactivity in response to intraperitoneal hypertonic NaCl in both Agt−/− mice and WT mice. Polyethylene glycol treatment increased Fos-immunoreactivity in the subfornical organ, OVLT, and supraoptic nuclei in WT mice but only increased Fos-immunoreactivity in the supraoptic nucleus in Agt−/− mice. These data show that brain angiotensin is not essential for the adequate functioning of neural pathways mediating osmoregulatory thirst. However, angiotensin II of either peripheral or central origin is probably necessary for thirst and salt appetite that results from hypovolemia.

Salt appetite is suppressed by interference with angiotensin II and aldosterone

1986 ◽  
Vol 251 (4) ◽  
pp. R762-R768 ◽  
Author(s):  
R. R. Sakai ◽  
S. Nicolaidis ◽  
A. N. Epstein
Keyword(s):  
Angiotensin Ii ◽  
Food Intake ◽  
Sodium Excretion ◽  
Salt Appetite ◽  
Mineralocorticoid Receptors ◽  
Sodium Depletion ◽  
Ru 28318 ◽  
Ingestive Behaviors ◽  
Captopril Treatment

Blockade of central but not peripheral mineralocorticoid receptors, with the antimineralocorticoid RU-28318, reduces but does not suppress salt appetite aroused by sodium depletion in the rat. When central mineralocorticoid blockade is combined with captopril treatment to prevent formation of endogenous angiotensin II the appetite is completely suppressed. Suppression of the appetite occurred without changes in the animals' spontaneous ingestive behaviors, sodium excretion, or insulin-induced food intake. These results demonstrate that a synergy of angiotensin II and aldosterone is responsible for the expression of depletion-induced salt appetite in the rat.

Interference with central actions of angiotensin II suppresses sodium appetite

1986 ◽  
Vol 250 (2) ◽  
pp. R250-R259 ◽  
Author(s):  
M. L. Weiss ◽  
K. E. Moe ◽  
A. N. Epstein
Keyword(s):  
Angiotensin Ii ◽  
Intracerebroventricular Injection ◽  
Compelling Evidence ◽  
Angiotensin I ◽  
Sodium Deficiency ◽  
Sodium Appetite ◽  
Intracerebroventricular Infusion ◽  
Central Actions ◽  
Ingestive Behaviors ◽  
The Brain

We have proposed that sodium appetite is aroused by a synergy in the brain of angiotensin II and aldosterone. This hypothesis was tested with 1) chronic intracerebroventricular infusion of captopril, which blocks the conversion of angiotensin I to angiotensin II, or 2) intracerebroventricular injection of eight-substituted analogues of angiotensin II, which block its receptors. Both treatments resulted in a suppression of the sodium appetite induced by sodium deficiency. The suppression was specific for the deficiency-induced appetite, because spontaneous ingestive behaviors were not changed nor was sodium excretion. In addition, the rats continued to express a sodium appetite aroused by pharmacological doses of deoxycorticosterone acetate when they received the highest dose of chronic intracerebroventricular captopril. These results offer compelling evidence for the idea that angiotensin II action in the brain is necessary for expression of sodium appetite.

Effect of adrenocorticotrophic hormone on sodium appetite in mice

1999 ◽  
Vol 277 (4) ◽  
pp. R1033-R1040 ◽  
Author(s):  
D. A. Denton ◽  
J. R. Blair-West ◽  
M. I. McBurnie ◽  
J. A. P. Miller ◽  
R. S. Weisinger ◽  
...  
Keyword(s):  
Sodium Intake ◽  
Sodium Content ◽  
Adrenocorticotrophic Hormone ◽  
Sodium Appetite ◽  
Corticotrophin Releasing Factor ◽  
Intracerebroventricular Infusion ◽  
Thymus Weight ◽  
Body Sodium ◽  
Voluntary Intake ◽  
Total Body

A main vector of the effects of stress is secretion of corticotrophin releasing factor (CRF), adrenocorticotrophin (ACTH), and adrenal steroids. Systemic administration of ACTH (2.8 μg/day sc) for 7 days in BALB/c mice caused a very large increase of voluntary intake of 0.3 M NaCl equivalent to turnover of total body sodium content each day. Intracerebroventricular infusion of ACTH (20 ng/day) had no effect. Intracerebroventricular infusion of ovine CRF (10 ng/h for 7 days) caused an increase of sodium intake. The large sodium appetite-stimulating effect of systemic ACTH was not influenced by concurrent systemic infusion of captopril (2 mg/day). Induction of stress by immobilization of mice on a running wheel caused an increase in Na appetite associated with a 50% decrease of thymus weight, indicative of corticosteroid effects. The present data suggest that stress and the hormone cascade initiated by stress evoke a large sodium appetite in mice, which may be an important survival mechanism in environmental conditions causing stress.

Sign in / Sign up

Export Citation Format

Share Document