Central infusion of the AT1 receptor antagonist losartan inhibits thirst but not sodium appetite in cattle

1997 ◽  
Vol 272 (6) ◽  
pp. R1940-R1945 ◽  
Author(s):  
J. R. Blair-West ◽  
D. A. Denton ◽  
M. J. McKinley ◽  
R. S. Weisinger
Keyword(s):  
Water Intake ◽  
Salt Intake ◽  
Sodium Intake ◽  
High Water ◽  
Salt Appetite ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Water Restriction ◽  
Sodium Appetite ◽  
High Water Intake

Experiments in cattle compared the effects of intracerebroventricular (i.c.v.) infusions of losartan and PD-123319 on water intake caused by water restriction, i.c.v. infusion of hypertonic NaCl, or i.c.v. infusion of angiotensin II (ANG II). The effects of these receptor antagonists on sodium intake caused by sodium depletion were also examined. Losartan infusion caused dose-dependent inhibition of the high water intake caused by the physiological stimulus of water restriction or by ANG II infusion but did not affect salt appetite. PD-123319 infused at equimolar or greater (in ANG II experiments) doses did not affect water intake or salt intake due to sodium depletion. The results of these i.c.v. infusion experiments confirm our earlier proposal that the physiological regulation of water intake in cattle may be mediated by ANG II acting centrally via AT1 receptors. The dose of losartan that inhibited thirst in cattle did not inhibit sodium appetite, nor did an equimolar dose of PD-123319.

scholarly journals Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT1) receptors

2008 ◽  
Vol 295 (5) ◽  
pp. R1539-R1545 ◽  
Author(s):  
Eric Lazartigues ◽  
Puspha Sinnayah ◽  
Ginette Augoyard ◽  
Claude Gharib ◽  
Alan Kim Johnson ◽  
...  
Keyword(s):  
Water Intake ◽  
Salt Intake ◽  
Sodium Intake ◽  
Third Ventricle ◽  
Model Neuron ◽  
Neuron Specific Enolase ◽  
Salt Appetite ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Salt Consumption

To address the relative contribution of central and peripheral angiotensin II (ANG II) type 1A receptors (AT1A) to blood pressure and volume homeostasis, we generated a transgenic mouse model [neuron-specific enolase (NSE)-AT1A] with brain-restricted overexpression of AT1A receptors. These mice are normotensive at baseline but have dramatically enhanced pressor and bradycardic responses to intracerebroventricular ANG II or activation of endogenous ANG II production. Here our goal was to examine the water and sodium intake in this model under basal conditions and in response to increased ANG II levels. Baseline water and NaCl (0.3 M) intakes were significantly elevated in NSE-AT1A compared with nontransgenic littermates, and bolus intracerebroventricular injections of ANG II (200 ng in 200 nl) caused further enhanced water intake in NSE-AT1A. Activation of endogenous ANG II production by sodium depletion (10 days low-sodium diet followed by furosemide, 1 mg sc) enhanced NaCl intake in NSE-AT1A mice compared with wild types. Fos immunohistochemistry, used to assess neuronal activation, demonstrated sodium depletion-enhanced activity in the anteroventral third ventricle region of the brain in NSE-AT1A mice compared with control animals. The results show that brain-selective overexpression of AT1A receptors results in enhanced salt appetite and altered water intake. This model provides a new tool for studying the mechanisms of brain AT1A-dependent water and salt consumption.

scholarly journals Signal Transduction of Mineralocorticoid and Angiotensin II Receptors in the Central Control of Sodium Appetite: A Narrative Review

2021 ◽  
Vol 22 (21) ◽  
pp. 11735
Author(s):  
Michele Iovino ◽  
Tullio Messana ◽  
Giuseppe Lisco ◽  
Aldo Vanacore ◽  
Vito Angelo Giagulli ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Salt Intake ◽  
Sodium Intake ◽  
Zona Glomerulosa ◽  
Narrative Review ◽  
Mitogen Activated Protein Kinase ◽  
Central Control ◽  
Ang Ii ◽  
Sodium Appetite ◽  
Mesh Terms

Sodium appetite is an innate behavior occurring in response to sodium depletion that induces homeostatic responses such as the secretion of the mineralocorticoid hormone aldosterone from the zona glomerulosa of the adrenal cortex and the stimulation of the peptide hormone angiotensin II (ANG II). The synergistic action of these hormones signals to the brain the sodium appetite that represents the increased palatability for salt intake. This narrative review summarizes the main data dealing with the role of mineralocorticoid and ANG II receptors in the central control of sodium appetite. Appropriate keywords and MeSH terms were identified and searched in PubMed. References to original articles and reviews were examined, selected, and discussed. Several brain areas control sodium appetite, including the nucleus of the solitary tract, which contains aldosterone-sensitive HSD2 neurons, and the organum vasculosum lamina terminalis (OVLT) that contains ANG II-sensitive neurons. Furthermore, sodium appetite is under the control of signaling proteins such as mitogen-activated protein kinase (MAPK) and inositol 1,4,5-thriphosphate (IP3). ANG II stimulates salt intake via MAPK, while combined ANG II and aldosterone action induce sodium intake via the IP3 signaling pathway. Finally, aldosterone and ANG II stimulate OVLT neurons and suppress oxytocin secretion inhibiting the neuronal activity of the paraventricular nucleus, thus disinhibiting the OVLT activity to aldosterone and ANG II stimulation.

Circulating angiotensin II mediates sodium appetite in adrenalectomized rats

2001 ◽  
Vol 281 (3) ◽  
pp. R723-R729 ◽  
Author(s):  
G. H. M. Schoorlemmer ◽  
A. K. Johnson ◽  
R. L. Thunhorst
Keyword(s):  
Intravenous Infusion ◽  
Sodium Intake ◽  
Peripheral Circulation ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Sodium Appetite ◽  
Brain Ventricle ◽  
The Brain ◽  
Adrenalectomized Rats

We investigated the role of circulating ANG II in sodium appetite after adrenalectomy. Adrenalectomized rats deprived of their main access to sodium (0.3 M NaCl) for 9 h drank 14.1 ± 1.5 ml of the concentrated saline solution in 2 h of access. Intravenous infusion of captopril (2.5 mg/h) during the last 5 h of sodium restriction reduced sodium intake by 77 ± 12% ( n = 5) without affecting the degree of sodium depletion and hypovolemia incurred during deprivation. Functional evidence indicates that this dose of captopril blocked production of ANG II in the peripheral circulation, but not in the brain; that is, injection of ANG I into the lateral brain ventricle stimulated intake of both water and 0.3 M NaCl. Intravenous infusion of ANG II (starting 10–15 min before 0.3 M NaCl became available) in adrenalectomized, captopril-treated rats restored both sodium intake and blood pressure to values seen in rats not treated with captopril. Longer (20 h) infusions of captopril in 22-h sodium-restricted rats also blocked sodium appetite, but reduced or prevented sodium depletion. Intravenous infusion of ANG II after these long captopril infusions stimulated sodium intake, but intake was less than in controls not treated with captopril. These results indicate that most or all of the sodium appetite of adrenalectomized rats is mediated by circulating ANG II.

Evidence that brain angiotensin II is involved in both thirst and sodium appetite in baboons

1998 ◽  
Vol 275 (5) ◽  
pp. R1639-R1646 ◽  
Author(s):  
J. R. Blair-West ◽  
K. D. Carey ◽  
D. A. Denton ◽  
R. S. Weisinger ◽  
R. E. Shade
Keyword(s):  
Water Intake ◽  
Daily Intake ◽  
Primate Species ◽  
Ang Ii ◽  
Water Restriction ◽  
High Intake ◽  
Sodium Appetite ◽  
The Brain ◽  
Na Depletion ◽  
Day By Day

The roles of ANG II in the brain mechanisms subserving thirst and Na appetite in baboons were investigated by chronic intracerebroventricular infusions of ANG II and AT1-receptor antagonists using subcutaneous miniosmotic pumps and by oral administration of captopril. ANG II at 3 or 5 μg/h for 7 days increased water intake from 2,455 ± 107 to 7,052 ± 562 ml/day by day 6 and 300 mM NaCl intake from 8.3 ± 1.1 to 275 ± 87 mmol/day by day 5. Concurrent intracerebroventricular losartan (300 μg/h) did not substantially reduce these responses, but they were abolished by intracerebroventricular ZD-7155 (50 μg/h). The increase of 300 mM NaCl intake when it was offered after intramuscular injection of furosemide, 2 mg ⋅ kg−1 ⋅ day−1for 3 days, was unaltered by intracerebroventricular losartan (300 μg/h) but was reduced by intracerebroventricular ZD-7155 (50 μg/h) infused throughout Na depletion/repletion; oral captopril (1 g, 3 and 18 h before access to 300 mM NaCl) also reduced NaCl intake. Restriction of water intake to 25% of daily intake for 3 days caused a high intake of water on day 4, and this was reduced by intracerebroventricular losartan (300 μg/h) infused throughout the period of water restriction/rehydration. These novel results in a primate species suggest that brain ANG II is involved in both thirst and Na appetite, acting via AT1 receptors.

Psychosis-related polydipsia and chronic hyponatremia – A case report

2016 ◽  
Vol 33 (S1) ◽  
pp. S578-S578
Author(s):  
F. Gonçalves Godinho ◽  
A.L. Melo ◽  
S. Marques ◽  
D. Barrocas
Keyword(s):  
Case Report ◽  
Water Intake ◽  
High Water ◽  
Psychotic Symptoms ◽  
Water Restriction ◽  
Psychogenic Polydipsia ◽  
Behavioral Measures ◽  
Severe Hyponatremia ◽  
High Water Intake ◽  
Competing Interest

IntroductionPsychogenic polydipsia has an estimated prevalence of 6–20% in psychiatric population. Although first described in the 1930s, there are few studies addressing this problem and its management. The high water intake can lead to severe hyponatremia with a mortality rate high enough to merit clinical concern.AimsReport a case of a schizophrenic patient with psychogenic polydipsia and hyponatremia.MethodsRetrospective review of the clinical file and literature research on this topic.ResultsA 41-year-old man with a long-term schizophrenia presented to the emergency room (ER) with exacerbation of psychotic symptoms. In the prior 24 months, he had stopped medication and began excessive water intake (5 to 10 L/day). He presented with auditory hallucinations, passivity phenomena and persecutory and other delusional thoughts that justified this behavior – “The water will end; I have to stock it, like camels do”. Presently he had an asymptomatic hyponatremia (128 mg/dL), but 6 months before he had been admitted in the ER with vomiting, altered state of consciousness and convulsions secondary to severe hyponatremia (108 mg/dL). During the present hospitalization, organic causes of hyponatremia were excluded and he was started on behavioral measures and antipsychotics. The psychotic symptoms improved and there was no need for water restriction after the first week, with restored natremia values on discharge.ConclusionsWith this case report we intended to raise awareness on this potentially fatal condition that despite its prevalence has no defined diagnostic criteria, nor established controlled trials concerning the effectiveness of treatments.Disclosure of interestThe authors have not supplied their declaration of competing interest.

scholarly journals Circumventricular organs and ANG II-induced salt appetite: blood pressure and connectivity

2000 ◽  
Vol 279 (6) ◽  
pp. R2277-R2286 ◽  
Author(s):  
Douglas A. Fitts ◽  
Elizabeth M. Starbuck ◽  
Alexandra Ruhf
Keyword(s):  
Blood Pressure ◽  
Water Intake ◽  
Femoral Vein ◽  
Circumventricular Organs ◽  
Subfornical Organ ◽  
Salt Appetite ◽  
Ang Ii ◽  
Sodium Depletion ◽  
Apparent Contradiction ◽  
Organum Vasculosum Laminae Terminalis

A lesion of the subfornical organ (SFO) may reduce sodium depletion-induced salt appetite, which is largely dependent on ANG II, and yet ANG II infusions directly into SFO do not provoke salt appetite. Two experiments were designed to address this apparent contradiction. In experiment 1 sustained infusions of ANG II into SFO did not produce a sustained elevation of blood pressure, and neither a reduction of blood pressure alone with minoxidil and captopril nor a reduction of both blood pressure and volume with furosemide and captopril enhanced salt appetite. Infusions of ANG II in the organum vasculosum laminae terminalis (OVLT) did evoke salt appetite without raising blood pressure. In experiment 2 knife cuts of the afferent and efferent fibers of the rostroventral pole of the SFO abolished water intake during an infusion of ANG II into the femoral vein but failed to reduce salt appetite during an infusion of ANG II into the OVLT. We conclude that 1) hypertension does not account for the failure of infusions of ANG II in the SFO to generate salt appetite and 2) the OVLT does not depend on its connectivity with the SFO to generate salt appetite during ANG II infusions.

The effect of increasing the salt intake of pregnant dairy cows on the salt appetite and growth of their calves

2003 ◽  
Vol 77 (1) ◽  
pp. 181-185 ◽  
Author(s):  
M. O. Mohamed ◽  
C. J. C. Phillips
Keyword(s):  
Birth Weight ◽  
Dairy Cows ◽  
Dry Matter ◽  
Neonatal Period ◽  
Salt Intake ◽  
Sodium Intake ◽  
Late Pregnancy ◽  
Salt Appetite ◽  
High Sodium ◽  
Sodium Appetite

AbstractAn increased sodium appetite has been demonstrated in cattle following supplementation with sodium in the neonatal period, but it is unclear whether the sodium appetite of calves can be influenced in utero by the dam’s sodium intake during pregnancy. Twenty-two non-lactating, pregnant dairy cows received either a diet of silage and concentrates or the same diet with 70 g NaCl per day added to it for the last 2 months of pregnancy. The sodium supplement increased the birth weight of their calves but after 6 weeks there was no difference between treatments in calf weight. In addition to milk, calves in both treatments were offered a choice of concentrates with normal or high sodium concentrations (5·8 and 10·8 g/kg dry matter, respectively). Calves from the cows that had received supplementary sodium during pregnancy ate more of the high sodium concentrate than calves from cows without the sodium supplement, demonstrating that sodium appetite could be entrained by the sodium intake of the dam during late pregnancy.

Salt appetite in rat pups: ontogeny of angiotensin II-aldosterone synergy

1991 ◽  
Vol 260 (2) ◽  
pp. R421-R429 ◽  
Author(s):  
C. I. Thompson ◽  
A. N. Epstein
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Salt Intake ◽  
Neural Mechanisms ◽  
Salt Appetite ◽  
Ang Ii ◽  
Rat Pups ◽  
Effective Doses ◽  
Old Rats ◽  
Individual Actions

Preweanling rats were tested to determine whether angiotensin II (ANG II) and aldosterone (Aldo) act synergistically to enhance salt appetite at 12 and 17 days. Twelve-day-old pups received one of four hormone treatments in four doses: 1) ANG II only [1, 2, 10, or 100 ng pulse intracerebroventricular (icv)], 2) Aldo only (1, 2, 10, or 40 micrograms/day sc), 3) Aldo + ANG II (four individual doses combined), or 4) vehicle. Seventeen-day-old rats received the same treatments in two doses (2 or 100 ng ANG II; 2 or 40 micrograms Aldo). Pups were presatiated with milk through anterior oral catheters and then given either 4% NaCl or water for 30 min. Intake was assessed by body weight change. At both ages, ANG II enhanced salt (and water) intake, and Aldo enhanced salt (but not water) intake. Minimum effective doses were comparable to those reported for adults. ANG II-Aldo synergy was absent at 12 days and present at 17 days, when salt intake was 590% greater than the summed intakes evoked by ANG II and Aldo alone. The neural mechanisms for ANG II-Aldo synergy thus mature later than those mediating the hormone's individual actions in arousing salt appetite.

Converting-enzyme inhibition abolishes polydipsia induced by dietary NaCl and K depletion

1990 ◽  
Vol 258 (5) ◽  
pp. F1164-F1172
Author(s):  
A. J. McKay ◽  
C. D. Poirier ◽  
L. N. Peterson
Keyword(s):  
Water Intake ◽  
Enzyme Inhibitor ◽  
Pressor Response ◽  
Plasma Renin ◽  
High Water ◽  
Ang Ii ◽  
Converting Enzyme ◽  
Daily Water Intake ◽  
High Water Intake ◽  
Converting Enzyme Inhibition

The present studies were designed to test the hypothesis that angiotensin II (ANG II) mediates nonosmotic thirst in animals fed the low-NaCl K-free diet by preventing the increased generation of ANG II using the converting-enzyme inhibitor, enalapril. Animals were fed either a control salt or low-NaCl K-free diet and were treated with or without enalapril. Water intake in rats fed the low-NaCl K-free diet increased more than twofold on day 3 and remained elevated over the 10-day period of study. Treatment with enalapril (40 mg.kg-1.day-1) 1) prevented the striking rise in plasma renin activity in rats fed the low-NaCl K-free diet, 2) led to complete blockade of the pressor response to a 50-ng injection of angiotensin I but not ANG II, 3) did not affect daily water intake in rats consuming the control salt diet, 4) did not reduce basal water intake in rats fed the low-NaCl K-free diet below values measured in control animals, and 5) did not abolish water intake in response to osmotic stimulation. However, enalapril treatment abolished the increase in water intake that occurs in animals fed the low-NaCl K-free diet. In a double crossover study using two groups of rats fed the low-NaCl K-free diet, enalapril prevented increased water intake in rats initially fed the low-NaCl K-free diet and rapidly inhibited increased water intake in rats fed the low-NaCl K-free diet after the high water intake had been established.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Positive and Negative Aspects of Sodium Intake in Dialysis and Non-Dialysis CKD Patients

Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 951
Author(s):  
Yasuyuki Nagasawa
Keyword(s):  
Blood Pressure ◽  
Nutritional Status ◽  
Water Intake ◽  
Salt Intake ◽  
Sodium Intake ◽  
Extracellular Fluid ◽  
Sodium Restriction ◽  
Dialysis Patients ◽  
Positive Effects ◽  
Volume Blood

Sodium intake theoretically has dual effects on both non-dialysis chronic kidney disease (CKD) patients and dialysis patients. One negatively affects mortality by increasing proteinuria and blood pressure. The other positively affects mortality by ameliorating nutritional status through appetite induced by salt intake and the amount of food itself, which is proportional to the amount of salt under the same salty taste. Sodium restriction with enough water intake easily causes hyponatremia in CKD and dialysis patients. Moreover, the balance of these dual effects in dialysis patients is likely different from their balance in non-dialysis CKD patients because dialysis patients lose kidney function. Sodium intake is strongly related to water intake via the thirst center. Therefore, sodium intake is strongly related to extracellular fluid volume, blood pressure, appetite, nutritional status, and mortality. To decrease mortality in both non-dialysis and dialysis CKD patients, sodium restriction is an essential and important factor that can be changed by the patients themselves. However, under sodium restriction, it is important to maintain the balance of negative and positive effects from sodium intake not only in dialysis and non-dialysis CKD patients but also in the general population.

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