Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 8 de 8
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
Horm Behav ; 118: 104658, 2020 02.
Artigo em Inglês | MEDLINE | ID: mdl-31874139

RESUMO

The aim of the present study was to determine whether the TRPV1 channel is involved in the onset of sodium appetite. For this purpose, we used TRPV1-knockout mice to investigate sodium depletion-induced drinking at different times (2/24 h) after furosemide administration combined with a low sodium diet (FURO-LSD). In sodium depleted wild type and TRPV1 KO (SD-WT/SD-TPRV1-KO) mice, we also evaluated the participation of other sodium sensors, such as TPRV4, NaX and angiotensin AT1-receptors (by RT-PCR), as well as investigating the pattern of neural activation shown by Fos immunoreactivity, in different nuclei involved in hydromineral regulation. TPRV1 SD-KO mice revealed an increased sodium preference, ingesting a higher hypertonic cocktail in comparison with SD-WT mice. Our results also showed in SD-WT animals that SFO-Trpv4 expression increased 2 h after FURO-LSD, compared to other groups, thus supporting a role of SFO-Trpv4 channels during the hyponatremic state. However, the SD-TPRV1-KO animals did not show this early increase, and maybe as a consequence drank more hypertonic cocktail. Regarding the SFO-NaX channel expression, in both genotypes our findings revealed a reduction 24 h after FURO-LSD. In addition, there was an increase in the OVLT-NaX expression of SD-WT 24 h after FURO-LSD, suggesting the participation of OVLT-NaX channels in the appearance of sodium appetite, possibly as an anticipatory response in order to limit sodium intake and to induce thirst. Our work demonstrates changes in the expression of different osmo­sodium-sensitive channels at specific nuclei, related to the body sodium status in order to stimulate an adequate drinking.


Assuntos
Apetite/genética , Encéfalo/metabolismo , Dieta Hipossódica , Sódio na Dieta/administração & dosagem , Canais de Cátion TRPV/fisiologia , Animais , Apetite/efeitos dos fármacos , Dieta Hipossódica/efeitos adversos , Ingestão de Líquidos/efeitos dos fármacos , Ingestão de Líquidos/genética , Ingestão de Alimentos/efeitos dos fármacos , Ingestão de Alimentos/genética , Furosemida/farmacologia , Masculino , Camundongos , Camundongos da Linhagem 129 , Camundongos Endogâmicos C57BL , Camundongos Knockout , Sódio na Dieta/metabolismo , Canais de Cátion TRPV/genética , Canais de Cátion TRPV/metabolismo , Sede/efeitos dos fármacos , Sede/fisiologia
2.
J Neuroendocrinol ; 30(4): e12585, 2018 04.
Artigo em Inglês | MEDLINE | ID: mdl-29486102

RESUMO

Numerous studies demonstrate the significant role of central ß-endorphin and its receptor, the µ-opioid receptor (MOR), in sodium intake regulation. The present study aimed to investigate the possible relationship between chronic high-NaCl intake and brain endogenous MOR functioning. We examined whether short-term (4 days) obligatory salt intake (2% NaCl solution) in rats induces changes in MOR mRNA expression, G-protein activity and MOR binding capacity in brain regions involved in salt intake regulation. Plasma osmolality and electrolyte concentrations after sodium overload and the initial and final body weight of the animals were also examined. After 4 days of obligatory hypertonic sodium chloride intake, there was clearly no difference in MOR mRNA expression and G-protein activity in the median preoptic nucleus (MnPO). In the brainstem, MOR binding capacity also remained unaltered, although the maximal efficacy of MOR G-protein significantly increased. Finally, no significant alterations were observed in plasma osmolality and electrolyte concentrations. Interestingly, animals that received sodium gained significantly less weight than control animals. In conclusion, we found no significant alterations in the MnPO and brainstem in the number of available cell surface MORs or de novo syntheses of MOR after hypertonic sodium intake. The increased MOR G-protein activity following acute sodium overconsumption may participate in the maintenance of normal blood pressure levels and/or in enhancing sodium taste aversion and sodium overload-induced anorexia.


Assuntos
Encéfalo/efeitos dos fármacos , Receptores Opioides mu/metabolismo , Transdução de Sinais/efeitos dos fármacos , Cloreto de Sódio/administração & dosagem , Animais , Encéfalo/metabolismo , Área Pré-Óptica/efeitos dos fármacos , Área Pré-Óptica/metabolismo , Ratos , Ratos Sprague-Dawley
3.
Neuroscience ; 340: 521-529, 2017 01 06.
Artigo em Inglês | MEDLINE | ID: mdl-27856342

RESUMO

A single exposure to amphetamine induces neurochemical sensitization in striatal areas. The neuropeptide angiotensin II, through AT1 receptors (AT1-R) activation, is involved in these responses. However, amphetamine-induced alterations can be extended to extra-striatal areas involved in blood pressure control and their physiological outcomes. Our aim for the present study was to analyze the possible role for AT1-R in these events using a two-injection protocol and to further characterize the proposed AT1-R antagonism protocol. Central effect of orally administered AT1-R blocker (Candesartan, 3mg/kg p.o.×5days) in male Wistar rats was analyzed by spontaneous activity of neurons within locus coeruleus. In another group of animals pretreated with the AT1-R blocker or vehicle, sensitization was achieved by a single administration of amphetamine (5mg/kg i.p. - day 6) followed by a 3-week period off drug. On day 27, after receiving an amphetamine challenge (0.5mg/kg i.p.), we evaluated: (1) the sensitized c-Fos expression in locus coeruleus (LC), nucleus of the solitary tract (NTS), caudal ventrolateral medulla (A1) and central amygdala (CeAmy); and (2) the blood pressure response. AT1-R blockade decreased LC neurons' spontaneous firing rate. Moreover, sensitized c-Fos immunoreactivity in TH+neurons was found in LC and NTS; and both responses were blunted by the AT1-R blocker pretreatment. Meanwhile, no differences were found neither in CeAmy nor A1. Sensitized blood pressure response was observed as sustained changes in mean arterial pressure and was effectively prevented by AT1-R blockade. Our results extend AT1-R role in amphetamine-induced sensitization over noradrenergic nuclei and their cardiovascular output.


Assuntos
Anfetamina/farmacologia , Pressão Sanguínea/efeitos dos fármacos , Neurônios/efeitos dos fármacos , Receptor Tipo 1 de Angiotensina/metabolismo , Simpatomiméticos/farmacologia , Potenciais de Ação/efeitos dos fármacos , Potenciais de Ação/fisiologia , Bloqueadores do Receptor Tipo 1 de Angiotensina II/farmacologia , Animais , Pressão Sanguínea/fisiologia , Núcleo Central da Amígdala/citologia , Núcleo Central da Amígdala/efeitos dos fármacos , Núcleo Central da Amígdala/metabolismo , Locus Cerúleo/citologia , Locus Cerúleo/efeitos dos fármacos , Locus Cerúleo/metabolismo , Masculino , Bulbo/citologia , Bulbo/efeitos dos fármacos , Bulbo/metabolismo , Neurônios/citologia , Neurônios/metabolismo , Proteínas Proto-Oncogênicas c-fos/metabolismo , Distribuição Aleatória , Ratos Wistar , Núcleo Solitário/citologia , Núcleo Solitário/efeitos dos fármacos , Núcleo Solitário/metabolismo
4.
Neuroscience ; 297: 78-88, 2015 Jun 25.
Artigo em Inglês | MEDLINE | ID: mdl-25841323

RESUMO

Our aim was to analyze the participation of inhibitory and stimulatory signals in the temporal dissociation between sodium depletion (SD) induced by peritoneal dialysis (PD) and the appearance of sodium appetite (SA), particularly 2h after PD, when the rats are hypovolemic/natremic but SA is not evident. We investigated the effects of bilateral injections of the serotonin (5-HT) receptor antagonist, methysergide, into the lateral parabrachial nucleus (LPBN) on hypertonic NaCl and water intake 2h vs. 24h after PD. We also studied plasma renin activity (PRA) and aldosterone (ALDO) concentration 2h vs. 24h after PD. Additionally, we combined the analysis of brain Fos immunoreactivity (Fos-ir) with the detection of double immunoreactivity in 5HT and oxytocinergic (OT) cells 2h after PD. Bilateral LPBN injections of methysergide (4µg/200nl at each site) increased NaCl intake when tested 2h after PD compared to controls. We found a significant increase in PRA and ALDO concentration after PD but no differences between 2 and 24h after PD. We also found for the first time a significant increase 2h after PD in the number of Fos-ir neurons in the brainstem nuclei that have been shown to be involved in the inhibition of SA. In summary, the results show that 5HT-mechanisms in the LPBN modulate sodium intake during the delay of SA when the renin angiotensin aldosterone system (RAAS) is increased. In addition, the activation of brainstem areas previously associated with the satiety phase of SA is in part responsible for the temporal dissociation between SD and behavioral arousal.


Assuntos
Apetite/fisiologia , Encéfalo/metabolismo , Comportamento de Ingestão de Líquido/fisiologia , Sódio/metabolismo , Administração Oral , Aldosterona/sangue , Animais , Apetite/efeitos dos fármacos , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Glucose/administração & dosagem , Masculino , Metisergida/farmacologia , Proteínas Oncogênicas v-fos/metabolismo , Ocitocina/metabolismo , Núcleos Parabraquiais/efeitos dos fármacos , Ratos , Ratos Wistar , Renina/sangue , Solução Salina Hipertônica/administração & dosagem , Serotonina/metabolismo , Antagonistas da Serotonina/farmacologia , Fatores de Tempo , Equilíbrio Hidroeletrolítico
5.
Neuroscience ; 298: 120-36, 2015 Jul 09.
Artigo em Inglês | MEDLINE | ID: mdl-25872186

RESUMO

Exposure to an altered osmotic environment during a pre/postnatal period can differentially program the fluid intake and excretion pattern profile in a way that persists until adulthood. However, knowledge about the programming effects on the underlying brain neurochemical circuits of thirst and hydroelectrolyte balance, and its relation with behavioral outputs, is limited. We evaluated whether early voluntary intake of hypertonic NaCl solution may program adult offspring fluid balance, plasma vasopressin, neural activity, and brain vasopressin and angiotensinergic receptor type 1a (AT1a)-receptor gene expression. The manipulation (M) period covered dams from 1 week before conception until offspring turned 1-month-old. The experimental groups were (i) Free access to hypertonic NaCl solution (0.45 M NaCl), food (0.18% NaCl) and water [M-Na]; and (ii) Free access to food and water only [M-Ctrol]. Male offspring (2-month-old) were subjected to iv infusion (0.15 ml/min) of hypertonic (1.5M NaCl), isotonic (0.15M NaCl) or sham infusion during 20 min. Cumulative water intake (140 min) and drinking latency to the first lick were recorded from the start of the infusion. Our results indicate that, after systemic sodium overload, the M-Na group had increased water intake, and diminished neuronal activity (Fos-immunoreactivity) in the subfornical organ (SFO) and nucleus of the solitary tract. They also showed reduced relative vasopressin (AVP)-mRNA and AT1a-mRNA expression at the supraoptic nucleus and SFO, respectively. The data indicate that the availability of a rich source of sodium during the pre/postnatal period induces a long-term effect on drinking, neural activity, and brain gene expression implicated in the control of hydroelectrolyte balance.


Assuntos
Encéfalo/citologia , Ingestão de Líquidos/efeitos dos fármacos , Expressão Gênica/efeitos dos fármacos , Neurônios/metabolismo , Efeitos Tardios da Exposição Pré-Natal/fisiopatologia , Solução Salina Hipertônica/efeitos adversos , Fatores Etários , Animais , Animais Recém-Nascidos , Feminino , Seguimentos , Masculino , Gravidez , Ratos , Ratos Wistar , Receptor Tipo 1 de Angiotensina/genética , Receptor Tipo 1 de Angiotensina/metabolismo , Fatores de Tempo , Vasopressinas/genética , Vasopressinas/metabolismo , Equilíbrio Hidroeletrolítico/efeitos dos fármacos
6.
Physiol Behav ; 105(4): 1035-44, 2012 Feb 28.
Artigo em Inglês | MEDLINE | ID: mdl-22133520

RESUMO

Osmoregulatory mechanisms can be vulnerable to electrolyte and/or endocrine environmental changes during the perinatal period, differentially programming the developing offspring and affecting them even in adulthood. The aim of this study was to evaluate whether availability of hypertonic sodium solution during the perinatal period may induce a differential programming in adult offspring osmoregulatory mechanisms. With this aim, we studied water and sodium intake after Furosemide-sodium depletion in adult offspring exposed to hypertonic sodium solution from 1 week before mating until postnatal day 28 of the offspring, used as a perinatal manipulation model [PM-Na group]. In these animals, we also identified the cell population groups in brain nuclei activated by Furosemide-sodium depletion treatment, analyzing the spatial patterns of Fos and Fos-vasopressin immunoreactivity. In sodium depleted rats, sodium and water intake were significantly lower in the PM-Na group vs. animals without access to hypertonic sodium solution [PM-Ctrol group]. Interestingly, when comparing the volumes consumed of both solutions in each PM group, our data show the expected significant differences between both solutions ingested in the PM-Ctrol group, which makes an isotonic cocktail; however, in the PM-Na group there were no significant differences in the volumes of both solutions consumed after Furosemide-sodium depletion, and therefore the sodium concentration of total fluid ingested by this group was significantly higher than that in the PM-Ctrol group. With regard to brain Fos immunoreactivity, we observed that Furosemide-sodium depletion in the PM-Na group induced a higher number of activated cells in the subfornical organ, ventral subdivision of the paraventricular nucleus and vasopressinergic neurons of the supraoptic nucleus than in the PM-Ctrol animals. Moreover, along the brainstem, we found a decreased number of sodium depletion-activated cells within the nucleus of the solitary tract of the PM-Na group. Our data indicate that early sodium availability induces a long-term effect on fluid drinking and on the cell activity of brain nuclei involved in the control of hydromineral balance. These results also suggest that availability of a rich source of sodium during the perinatal period may provoke a larger anticipatory response in the offspring, activating the vasopressinergic system and reducing thirst after water and sodium depletion, as a result of central osmosensitive mechanism alterations.


Assuntos
Solução Salina Hipertônica/farmacologia , Equilíbrio Hidroeletrolítico/efeitos dos fármacos , Animais , Encéfalo/efeitos dos fármacos , Encéfalo/fisiologia , Ingestão de Líquidos/efeitos dos fármacos , Ingestão de Líquidos/fisiologia , Feminino , Furosemida/farmacologia , Masculino , Imagem Molecular/métodos , Imagem Molecular/estatística & dados numéricos , Gravidez , Ratos , Ratos Wistar , Sódio/deficiência , Sódio/metabolismo , Equilíbrio Hidroeletrolítico/fisiologia
7.
Regul Pept ; 167(2-3): 222-6, 2011 Apr 11.
Artigo em Inglês | MEDLINE | ID: mdl-21324347

RESUMO

In the present study, we investigated the degree to which ß-endorphin plays a role in the alpha 2-adrenergic/imidazoline receptor agonist attenuation of salt appetite. In order to evaluate whether the inhibitory action of clonidine (an α2-adrenergic/imidazoline receptor agonist) on induced sodium intake is mediated by the ß-endorphinergic system, we used a ß-endorphin deficient mouse line. ß-endorphin knockout (ßend(-/-)), heterozygous (ßend(+/-)) and wild-type (ßend(+/+)) mice were submitted to acute sodium depletion by a combined treatment of furosemide and low sodium diet and, 20h later, were administered with clonidine (0.5mg/kg). An hour later, the animals were subjected to a two-bottle choice test (water/2% NaCl). The results indicate that clonidine administration during the first stage of the test exerts an equivalent inhibition on sodium intake regardless of the genotype; however, in the final stage of the test, a reversal of the inhibitory response on induced sodium appetite becomes evident in the mice lacking ß-endorphin. Moreover no differences in dipsogenic response were observed between the genotypes. Considering these results and the fact that plasma half-life of clonidine at the dose administered is approximately 3h, it is possible to speculate that the inhibitory effect of clonidine on sodium appetite may be independent of ß-endorphin modulation during the first stage; however, the long-lasting inhibitory effect of clonidine may be mediated by the ß-endorphinergic system. This evidence supports the existence of adrenergic and ß-endorphinergic system interaction in the osmoregulatory response to achieve sodium balance.


Assuntos
Agonistas de Receptores Adrenérgicos alfa 2/farmacologia , Apetite/efeitos dos fármacos , Clonidina/farmacologia , Receptores de Imidazolinas/agonistas , Cloreto de Sódio na Dieta/farmacologia , beta-Endorfina/fisiologia , Animais , Clonidina/administração & dosagem , Ingestão de Líquidos/fisiologia , Furosemida/farmacologia , Camundongos , Camundongos Endogâmicos , Receptores Adrenérgicos alfa 2/metabolismo
8.
Neuroscience ; 142(2): 557-65, 2006 Oct 13.
Artigo em Inglês | MEDLINE | ID: mdl-16887279

RESUMO

The present study was performed to examine the role of the endogenous beta-endorphinergic system on blood pressure regulation, sympathetic and brain activity during body sodium overload. Beta-endorphin knockout (beta end-/-), heterozygous (beta end+/-) and wild-type (beta end+/+) mice were submitted for two weeks to either a normal- or a high-sodium diet (NSD and HSD, respectively), and systolic blood pressure (SBP), urinary catecholamines (as an index of sympathetic nervous system activity), and the brain pattern of Fos-like immunoreactivity (as a marker of neuronal activation) were evaluated in each group. HSD caused a significant increase in SBP in beta end-/- mutant mice compared with beta end+/+ mice kept in the same experimental conditions (P < 0.01), but no statistical differences were observed between beta end+/- and beta end+/+ on a HSD. Moreover, when animals from the three genetic lines were fed with a NSD no changes in SBP were evidenced. With regard to brain activity, beta end-/- mice maintained on a HSD showed a significant increase in Fos-like immunoreactive neurons in the median preoptic nucleus (P < 0.01) compared with beta end+/- and beta end+/+ animals. Additionally, beta end-/- mice had higher levels of urinary epinephrine excretion (P < 0.05) on a HSD in comparison to beta end+/+ and beta end+/- animals in the same experimental conditions. No differences, however, were registered in norepinephrine and dopamine urinary excretion in animals from the three genetic lines after two weeks on either a HSD or a NSD. In summary, our results indicate that the beta-endorphinergic system may play a part in the compensatory response to sodium overload, since the absence of beta-endorphin causes an increase in systolic blood pressure, and increases median preoptic nucleus neural activity and urinary epinephrine excretion.


Assuntos
Pressão Sanguínea/fisiologia , Encéfalo/metabolismo , Sódio na Dieta/metabolismo , beta-Endorfina/fisiologia , Análise de Variância , Animais , Comportamento Animal , Pressão Sanguínea/efeitos dos fármacos , Pressão Sanguínea/genética , Peso Corporal/efeitos dos fármacos , Peso Corporal/genética , Encéfalo/efeitos dos fármacos , Catecolaminas/urina , Creatinina/urina , Ingestão de Líquidos/efeitos dos fármacos , Ingestão de Líquidos/genética , Regulação da Expressão Gênica/efeitos dos fármacos , Regulação da Expressão Gênica/genética , Imuno-Histoquímica/métodos , Camundongos , Camundongos Knockout , Proteínas Proto-Oncogênicas c-fos/metabolismo , Sódio na Dieta/farmacologia , beta-Endorfina/deficiência
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA