Central angiotensin II induces sodium bicarbonate intake in the rat

The aim of this work was to test mineral preference in hydrated rats that received a pulse intracerebroventricular (icv(p)) injection of ANG II at a dipsogenic dose (50 ng). The icv(p) ANG II induced a four-fold higher ingestion of 0.15 M NaHCO(3) than of other mineral solutions at palatable concentrations (0.15 M NaCl, 0.05 mM CaCl(2) and 0.01 M KCl) in a five-bottle test with water available in a fifth bottle; water intake was not consistently high in this test. Contrary to what is predicted by the mineralocorticoid/angiotensin II synergy hypothesis, the 0.15 M NaCl intake in the five-bottle test was not enhanced by icvp ANG H preceded by deoxycorticosterone (DOCA) treatment (2.5 mg/day for 3 days); neither was the NaHCO(3) intake. This result contrasted with the vigorous ingestion of both isotonic sodium solutions, but mostly of NaCl, rather than of other fluids, by sodium-depleted (furosemide 10 mg sc + 24 h removal ambient sodium) rats in a sodium appetite test. The results suggest that mineralocorticoid combined to icv(p) ANG II does not simulate the sodium preference shown during sodium appetite. The results also show that a dipsogenic dose of central ANG II induces a reliable ingestion of isotonic sodium bicarbonate in the rat. (C) 2007 Elsevier Ltd. All rights reserved.

Central serotonergic and adrenergic/imidazoline inhibitory mechanisms on sodium and water intake

Recent studies have shown the existence of two important inhibitory mechanisms for the control of NaCl and water intake: one mechanism involves serotonin in the lateral parabrachial nucleus (LPBN) and the other depends on alpha(2)-adrenergic/imidazoline receptors probably in the forebrain areas. In the present study we investigated if alpha(2)-adrenergic/imidazoline and serotonergic inhibitory mechanisms interact to control NaCl and water intake. Male Holtzman rats with cannulas implanted simultaneously into the lateral ventricle (LV) and bilaterally into the LPBN were used. The ingestion of 0.3 M NaCl and water was induced by treatment with the diuretic furosemide (10 mg/kg of body weight)+the angiotensin converting enzyme inhibitor captopril (5 mg/kg) injected subcutaneously 1 h before the access of rats to water and 0.3 M NaCl. Intracerebroventricular (i.c.v.) injection of the alpha(1)-adrenergic/imidazoline agonist clonidine (20 nmol/l RI) almost abolished water (1.6 +/- 1.2, vs. vehicle: 7.5 +/- 2.2 ml/2 h) and 0.3 M NaCl intake (0.5 +/- 0.3, vs. vehicle: 2.2 0.8 ml/2 h). Similar effects were produced by bilateral injections of the 5HT(2a/2b) serotonergic agonist 2,5-dimetoxy-4-iodoamphetamine (DOI, 5 mug/0.2 mul each site) into the LPBN on water (3.6 +/- 0.9 ml/2 h) and 0.3 M NaCl intake (0.4 +/- 0.2 m1/2 h). Injection of the (alpha(2)-adrenergic/imidazoline antagonist idazoxan (320 nmol) i.c.v. completely blocked the effects of clonidine on water (8.4 +/- 1.5 ml/2 h) and NaCl intake (4.0 +/- 1.2 ml/2 h), but did not change the effects of LPBN injections of DOI on water (4.2 +/- 1.0 ml/2 h) and NaCl intake (0.7 +/- 0.2 ml/2 h). Bilateral injections of methysergide (4 mug/0.2 mul each site) into the LPBN increased 0.3 M NaCl intake (6.4 +/- 1.9 ml/2 h), not water intake. The inhibitory effect of i.c.v. clonidine on water and 0.3 M NaCl was still present after injections of methysergide into the LPBN (1.5 +/- 0.8 and 1.7 +/- 1.4 ml/2 h, respectively). The results show that the inhibitory effects of the activation of a,-adrenergic/imidazoline receptors in the forebrain are still present after blockade of the LPBN serotonergic mechanisms and vice versa for the activation of serotonergic mechanisms of the LPBN. Therefore, each system may act independently to inhibit NaCl and water intake. (C) 2002 Elsevier B.V. B.V. All rights reserved.

Effects of different doses of sodium monensin on feeding behaviour, dry matter intake variation and selective consumption of feedlot Nellore cattle

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

The control of sodium chloride intake: Functional relationship between hypothalamic inhibitory areas and amygdaloid complex stimulating areas

Sodium chloride intake was studied in rats submitted to different neurosurgical procedures. Intake decreased in animals submitted to bilateral destruction of the basolateral amygdaloid complex, and increased after the same animals were submitted to destruction of the anterior lateral hypothalamus, a procedure which is known to cause increased intake in intact rats. In the reverse experiment, where the anterior lateral hypothalamus was destroyed before the basolateral amygdaloid complex, the effect of increased sodium chloride intake induced by destruction of the hypothalamus overcame the decreased expected upon destruction of the amygdaloid complex. These results permit us to conclude that the hypothalamic areas which inhibit sodium chloride intake predominate over the stimulating areas of the amygdaloid complex in the control of sodium chloride intake. © 1981 ANKHO International Inc.

Sodium levels for Japanese quail at initial phases

The aim of this research was to determine the nutritional requirements of sodium for Japanese quail (Coturnix coturnix Japonica) during the periods of 1 to 21 d and 22 to 40 d of age, as well as to evaluate the residual effect on egg production and densitometry bone traits from 41 to 63 d. Two experiments were developed. Experiment 1: 360 Japanese quail were used, from 1 to 21 d of age. Treatments consisted of 5 sodium levels (0.06, 0.12, 0.18, 0.24, and 0.30%). Experiment 2: 240 Japanese quail were used, from 22 to 40 d. Treatments consisted of 5 sodium levels (0.04, 0.12, 0.20, 0.28, and 0.36%). In both experiments, weight gain, final weight, and feed conversion presented a quadratic trend, whereas water intake presented a linear trend. Treatments did not affect the densitometry of bone traits, although they presented a quadratic influence on tibia ash, calcium, and calcium: phosphorus ratio. Therefore, the nutritional requirement of sodium for Japanese quail from 1 to 21 d and from 22 to 40 d is 0.222% and 0.253%, respectively.

Feed restriction on performance and blood parameters of broilers fed diets with different sodium levels

The experiment was conducted to evaluate the effect of feed restriction and different sodium levels in the diet on the performance and hematological values (erythrocyte, hemoglobin, hematocrit, mean cell volume, mean cell hemoglobin, mean cell hemoglobin concentration and white blood cell) of broilers from 22 to 42 days of age. A completely randomized design was used in a 4 x 2 x 2 factorial (levels of sodium: 0.16%, 0.19%, 0.22% and 0.25%; with or without feed restriction; male and female), and two replicates of thirty broilers each. Sodium levels did not affect performance (p>0.05). Feed restriction resulted in increased feed intake and affected weight gain and feed conversion negatively (p<0.05). Better weight gain and feed conversion (p<0.05) were seen in male broilers. Hematological values were not affected by sodium levels, feed restriction or sex (p>0.05).

No relationship between subchronic fluoride intake and DNA damage in Wistar rats

Fluoride has been widely used in dentistry because it is an effective caries prophylactic agent. However, excess fluoride may represent a hazard to human health, especially by causing injury on the genetic apparatus. Genotoxicity tests form an important part of cancer research and risk assessment of potential carcinogens. In the current study, the potential DNA damage associated with exposure to fluoride was assessed by the single cell gel ( comet) assay in peripheral blood, oral mucosa and brain cells in vivo. Male Wistar rats were exposed to sodium fluoride (NaF) at a 0, 7 and 100 ppm dose for drinking water during 6 weeks. The results pointed out that NaF did not contribute to the DNA damage in all cellular types evaluated as depicted by the mean tail moment and tail intensity. These findings are clinically important since they represent an important contribution to the correct evaluation of the potential health risk associated with dental agents exposure. Copyright (C) 2004 S. Karger AG, Basel.

Urinary lithiasis and idiopathic hypercalciuria: the importance of dietary intake evaluation

PUSPOSE: To evaluate food intake of patients with urinary lithiasis and idiopathic hypercalciuria (IH). MATERIALS and METHODS: Between August 2007 and June 2008, 105 patients with lithiasis were distributed into 2 groups: Group 1 (n = 55) - patients with IH (urinary calcium excretion > 250 mg in women and 300 mg in men with normal serum calcium); Group 2 (n = 50) - normocalciuria (NC) patients . Inclusion criteria were: age over 18, normal renal function (creatinine clearance = 60 mL/min), absent proteinuria and negative urinary culture. Pregnant women, patients with some intestinal pathology, chronic diarrhea or using corticoids were excluded. The protocol of metabolic investigation was based on non-consecutive collection of two 24-hour samples for dosages of: calcium, sodium, uric acid, citrate, oxalate, magnesium and urinary volume. Food intake was evaluated through the quantitative method of Dietary Register of three days. RESULTS: Urinary excretion of calcium (433.33 ± 141.92 vs. 188.93 ± 53.09), sodium (280.08 ± 100.94 vs. 200.44.93 ± 65.81), uric acid (880.63 ± 281.50 vs. 646.74 ± 182.76) and magnesium (88.78 ± 37.53 vs. 64.34 ± 31.84) was significantly higher in the IH group in comparison to the NC group (p < 0.05). As regards the nutritional composition of food intake of IH and NC groups, there was no statistical significant difference in any nutrient evaluated. CONCLUSION: In our study, no difference was observed in the food intake of patients with urinary lithiasis and IH or NC.

Effect of sodium gluconate on performance, carcass characteristics, and intestinal morphometry of broilers from 22 to 42 days of age

O presente estudo teve por objetivo avaliar o efeito da utilização de níveis crescentes do gluconato de sódio sobre o desempenho, o rendimento de carcaça e de partes e a morfometria da mucosa intestinal de frangos de corte de 22 a 42 dias de idade. Foram utilizados 1200 frangos de corte da linhagem Cobb, distribuídos em um delineamento inteiramente casualizado, envolvendo cinco tratamentos (0,00; 0,10; 0,20; 0,30 e 0,40% de gluconato de sódio) com oito repetições de 30 aves cada parcela. As variáveis foram submetidas à análise de variância e em caso de significância estatística foram realizadas análises de regressão pelos modelos polinomial e quadrático. A inclusão do gluconato de sódio não afetou o desempenho e o rendimento de carcaça e de partes. Entretanto, exerceu efeito benéfico sobre a morfometria da mucosa intestinal do duodeno e do jejuno.

GABA(A) receptor activation in the lateral parabrachial nucleus induces water and hypertonic NaCl intake

Inhibitory serotonergic and cholecystokinergic mechanisms in the lateral parabrachial nucleus and central GABAergic mechanisms are involved in the regulation of water and NaCl intake. In the present study we investigated if the GABA(A) receptors in the lateral parabrachial nucleus are involved in the control of water, NaCl and food intake in rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally into the lateral parabrachial nucleus were used. Bilateral injections of muscimol (0.2 nmol/0.2 mu l) into the lateral parabrachial nucleus strongly increased 0.3 M NaCl (20.3 +/- 7.2 vs. saline: 2.6 +/- 0.9 ml/180 min) without changing water intake induced by the treatment with the diuretic furosemide combined with low dose of the angiotensin converting enzyme inhibitor captopril s.c. In euhydrated and satiated rats, bilateral lateral parabrachial nucleus injections of muscimol (0.2 and 0.5 nmol/0.2 0) induced 0.3 M NaCl intake (12.1 +/- 6.5 and 32.5 +/- 7.3 ml/180 min, respectively, vs. saline: 0.4 +/- 0.2 ml/180 min) and water intake (5.2 +/- 2.0 and 7.6 +/- 2.8 ml/ 180 min, respectively, vs. saline: 0.8 +/- 0.4 ml/180 min), but no food intake (2 +/- 0.4 g/240 min vs. saline: 1 +/- 0.3 g/240 min). Bilateral lateral parabrachial nucleus injections of the GABAA antagonist bicuculline (1.6 nmol/0.2 mu l) abolished the effects of muscimol (0.5 nmol/0.2 mu l) on 0.3 M NaCl and water intake. Muscimol (0.5 nmol/0.2 mu l) into the lateral parabrachial nucleus also induced a slight ingestion of water (4.2 +/- 1.6 ml/240 min vs. saline: 1.1 +/- 0.3 ml/240 min) when only water was available, a long lasting (for at least 2 h) increase on mean arterial pressure (14 +/- 4 mm Hg, vs. saline: -1 +/- 1 mm Hg) and only a tendency to increase urinary volume and Na+ and K+ renal excretion. Therefore the activation of GABAA receptors in the lateral parabrachial nucleus induces strong NaCl intake, a small ingestion of water and pressor responses, without changes on food intake. (c) 2005 Published by Elsevier Ltd on behalf of IBRO.

Interaction between arginine vasopressin and angiotensin II receptors in the central regulation of sodium balance

We speculated that the influence of lateral preoptic area (LPO) in sodium balance, involves arginine(8)-vasopressin (AVP) and angiotensin (ANG II) on Na+ uptake in LPO. Therefore, the present study investigated the effects of central administration of specific AVP and ANG 11 antagonists (d(CH2)(5)-Tyr (Me)-AVP (AAVP) and [Adamanteanacetyl(1), 0-ET-D-Tyr(2), Val(4), Aminobutyryl(6), Arg(8.9)]-AVP (ATAVP) antagonists of V-1 and V-2 receptors of AVP. Also the effects of losartan and CGP42112A (selective ligands of the AT(1) and AT(2) angiotensin receptors, respectively), was investigated on Na+ uptake and renal fluid and electrolyte excretion. After an acclimatization period of 7 days, the animals were maintained under tribromoethanol (200 mg/kg body weight, intraperitonial) anesthesia and placed in a Kopf stereotaxic instrument. Stainless guide cannula was implanted into the LPO. AAVP and ATAVP injected into the LPO prior to AVP produced a reduction in the NaCl intake. Both the AT(1) and AT(2) ligands administered into the LPO elicited a decrease in the NaCl intake induced by AVP injected into the LPO. AVP injection into the LPO increased sodium renal excretion, but this was reduced by prior AAVP administration. The ATAVP produced a decreased in the natriuretic effect of AVP. The losartan injected into LPO previous to AVP decreased the sodium excretion and the CGP 421122A also decreased the natriuretic effect of AVP. The AVP produced an antidiuresis effect that was inhibited by prior administration into LPO of the ATAVP. The AAVP produced no change in the antidiuretic effect of AVP. These results suggest that LPO are implicated in sodium balance that is mediated by V-1, V-2, AT(2) and AT(2) receptors. (c) 2005 Elsevier B.V All rights reserved.

Activation of alpha(2)-adrenergic receptors into the lateral parabrachial nucleus enhances NaCl intake in rats

Water and NaCl intake is strongly inhibited by the activation of alpha(2)-adrenergic receptors with clonidine or moxonidine (alpha(2)-adrenergic/imidazoline agonists) injected peripherally or into the forebrain and by serotonin and cholecystokinin in the lateral parabrachial nucleus (LPBN). Considering that alpha(2)-adrenergic receptors exist in the LPBN and the similar origin of serotonergic and adrenergic afferent pathways to the LPBN, in this study we investigated the effects of bilateral injections of moxonidine alone or combined with RX 821002 (alpha(2)- adrenergic antagonist) into the LPBN on 1.8% NaCl and water intake induced by the treatment with s.c. furosemide (10 mg/kg)+captopril (5 mg/kg). Additionally, we investigated if moxonidine into the LPBN would modify furosemide+captopril-induced c-fos expression in the forebrain. Male Holtzman rats with cannulas implanted bilaterally in the LPBN were used. Contrary to forebrain injections, bilateral LPBN injections of moxonidine (0.1, 0.5 and 1 nmol/0.2 mul) strongly increased furosemide+captopril-induced 1.8% NaCl intake (16.6 +/- 2.7, 44.5 +/- 3.2 and 44.5 +/- 4.3 ml/2 h, respectively, vs. vehicle: 6.9 +/- 1.5 ml/2 h). Only the high dose of moxonidine increased water intake (23.3 +/- 3.8 ml/2 h, vs. vehicle: 12.1 +/- 2.6 ml/2 h). Prior injections of RX 821002 (10 and 20 nmol/0.2 mu1) abolished the effect of moxonidine (0.5 nmol) on 1.8% NaCl intake. Moxonidine into the LPBN did not modify furosemide+captopril-induced c-fos expression in forebrain areas related to the control of fluid-electrolyte balance. The results show that the activation of LPBN a2-adrenergic receptors enhances furosemide+captopril-induced 1.8% NaCl and water intake. This enhancement was not related to prior alteration in the activity of forebrain areas as suggested by c-fos expression. Previous and present results indicate opposite roles for alpha(2-)adrenergic receptors in the control of sodium and water intake according to their distribution in the rat brain. (C) 2004 IBRO. Published by Elsevier Ltd. All rights reserved.

Interaction between brain L-type calcium channels and alpha(2)-adrenoceptors in the inhibition of sodium appetite

Calcium channels mediate the actions of many drugs. The present work investigated whether diltiazem, an L-type calcium channel blocker, alters the inhibition of sodium appetite induced by noradrenaline and the alpha(2)-adrenoceptor agonist clonidine. Adult male Holtzman rats (N=4-8) with cannula implanted into the third cerebral ventricle were submitted to sodium depletion {furosemide sc+24-h removal of ambiente sodium). Sodium depleted control animals that received 0.9% NaCl as vehicle injected intracerebroventricularly (i.c.v) ingested 13.0+/-1.5 ml/120 min of 1.8% NaCl. Intracerebroventricular injection of either noradrenaline (80 nmol) or clonidine (20 nmol) inhibited 1.8% NaCl intake from 70 to 90%. Prior i.c.v. injection of diltiazem (6-48 nmol) inhibited from 50 to 100% the effect of noradrenaline and clonidine in a dose-response manner. Diltiazem alone at 100 nmol inhibited, but at 50 nmol had no effect on, sodium appetite. The results suggest: (1) common ionic mechanisms involving calcium channels for the inhibition that noradrenaline and clonidine exert on sodium appetite and (2) a dual role for the benzothiazepine site of L-type calcium channels in the control of sodium appetite. (C) 2002 Elsevier B.V. B V. All rights reserved.

Activation of serotonergic 5-HT1A receptors in the lateral parabrachial nucleus increases NaCl intake

Previous studies using non-specific serotonergic agonists and antagonists have shown the importance of serotonergic inhibitory mechanisms in the lateral parabrachial nucleus (LPBN) for controlling sodium and water intake. In the present study, we investigated whether the serotonergic 5-HTIA receptor subtype in the LPBN participates in this control. Male Holtzman rats had cannulas implanted bilaterally into the LPBN. Bilateral injections of the 5-HTIA receptor agonist, 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT, 0.1, 1.25, and 2.5 mu g/ 0.2 mu l), into the LPBN enhanced 0.3 M NaCl and water intake of rats injected subcutaneously with the diuretic furosemide (10 mg/kg bw) and a low dose of the angiotensin-converting enzyme inhibitor, captopril (5 mg/kg bw). The increase in NaCl intake produced by 8-OH-DPAT injections was reduced in dose-related manner by pre-treating the LPBN with the selective 5-HTIA serotonergic antagonist, WAY-100635 (WAY, I and 2 mu g/0.2 mu l). In contrast, WAY did not affect water intake produced by 8-OH-DPAT. WAY-100635 injected alone into the LPBN had no effect on NaCl ingestion. Injections of 8-OH-DAPT (0.1 mu g/0.2 mu l) into the LPBN also increased 0.3 M NaCl intake induced by 24-h sodium depletion (furosemide, 20 mg/kg bw plus 24 h of sodium-free diet). Serotonin (5-HT, 20 mu g/0.2 mu l) injected alone or combined with 8-OH-DPAT into the LPBN reduced 24-h sodium depletion-induced 0.3 M NaCl intake. Therefore, the activation of serotonergic 5-HTIA receptors in the LPBN increases stimulated hypertonic NaCl and water intake, while 5-HT injections into the LPBN reduce NaCl intake and prevent the effects of serotonergic 5-HTIA receptor activation. (c) 2005 Elsevier B.V. All rights reserved.