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1.
Hypertens Res ; 2020 May 27.
Artigo em Inglês | MEDLINE | ID: mdl-32461634

RESUMO

Intracerebroventricular (icv) injection of hydrogen peroxide (H2O2) or the increase of endogenous H2O2 centrally produced by catalase inhibition with 3-amino-1,2,4-triazole (ATZ) injected icv reduces the pressor responses to central angiotensin II (ANG II) in normotensive rats. In the present study, we investigated the changes in the arterial pressure and in the pressor responses to ANG II icv in spontaneously hypertensive rats (SHRs) and 2-kidney, 1-clip (2K1C) hypertensive rats treated with H2O2 injected icv or ATZ injected icv or intravenously (iv). Adult male SHRs or Holtzman rats (n = 5-10/group) with stainless steel cannulas implanted in the lateral ventricle were used. In freely moving rats, H2O2 (5 µmol/1 µl) or ATZ (5 nmol/1 µl) icv reduced the pressor responses to ANG II (50 ng/1 µl) icv in SHRs (11 ± 3 and 17 ± 4 mmHg, respectively, vs. 35 ± 6 mmHg) and 2K1C hypertensive rats (3 ± 1 and 16 ± 3 mmHg, respectively, vs. 26 ± 2 mmHg). ATZ (3.6 mmol/kg of body weight) iv alone or combined with H2O2 icv also reduced icv ANG II-induced pressor response in SHRs and 2K1C hypertensive rats. Baseline arterial pressure was also reduced (-10 to -15 mmHg) in 2K1C hypertensive rats treated with H2O2 icv and ATZ iv alone or combined and in SHRs treated with H2O2 icv alone or combined with ATZ iv. The results suggest that exogenous or endogenous H2O2 acting centrally produces anti-hypertensive effects impairing central pressor mechanisms activated by ANG II in SHRs or 2K1C hypertensive rats.

2.
Brain Res Bull ; 153: 266-272, 2019 11.
Artigo em Inglês | MEDLINE | ID: mdl-31545999

RESUMO

Intracerebroventricular (icv) injection of hydrogen peroxide (H2O2), a reactive oxygen species, or the blockade of catalase (enzyme that degrades H2O2 into H2O and O2) with icv injection of 3-amino-1,2,4-triazole (ATZ) reduces the pressor effects of angiotensin II also injected icv. In the present study, we investigated the effects of ATZ injected icv or intravenously (iv) on the pressor responses induced by icv injections of the cholinergic agonist carbachol, which similar to angiotensin II induces pressor responses that depend on sympathoexcitation and vasopressin release. In addition, the effects of H2O2 icv on the pressor responses to icv carbachol were also tested to compare with the effects of ATZ. Normotensive non-anesthetized male Holtzman rats (280-300 g, n = 8-9/group) with stainless steel cannulas implanted in the lateral ventricle were used. Previous injection of ATZ (5 nmol/1 µl) or H2O2 (5 µmol/1 µl) icv similarly reduced the pressor responses induced by carbachol (4 nmol/1 µl) injected icv (13 ± 4 and 12 ± 4 mmHg, respectively, vs. vehicle + carbachol: 30 ± 5 mmHg). ATZ (3.6 mmol/kg of body weight) injected iv also reduced icv carbachol-induced pressor responses (21 ± 2 mmHg). ATZ icv or iv and H2O2 icv injected alone produced no effect on baseline arterial pressure. The treatments also produced no significant change of heart rate. The results show that ATZ icv or iv reduced the pressor responses to icv carbachol, suggesting that endogenous H2O2 acting centrally inhibits the pressor mechanisms (sympathoactivation and/or vasopressin release) activated by central cholinergic stimulation.

3.
Brain Res Bull ; 144: 14-20, 2019 01.
Artigo em Inglês | MEDLINE | ID: mdl-30391542

RESUMO

Central cholinergic activation stimulates water intake, but also NaCl intake when the inhibitory mechanisms are blocked with injections of moxonidine (α2 adrenergic/imidazoline agonist) into the lateral parabrachial nucleus (LPBN). In the present study, we investigated the involvement of central M1 and M2 muscarinic receptors on NaCl intake induced by pilocarpine (non-selective muscarinic agonist) intraperitoneally combined with moxonidine into the LPBN or by muscimol (GABAA agonist) into the LPBN. Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN and in the lateral ventricle were used. Pirenzepine (M1 muscarinic antagonist, 1 nmol/1 µl) or methoctramine (M2 muscarinic antagonist, 50 nmol/1 µL) injected intracerebroventricularly (i.c.v.) reduced 0.3 M NaCl and water intake in rats treated with pilocarpine (0.1 mg/100 g of body weight) injected intraperitoneally combined with moxonidine (0.5 nmol/0.2 µL) into the LPBN. In rats treated with muscimol (0.5 nmol/0.2 µL) into the LPBN, methoctramine i.c.v. also reduced 0.3 M NaCl and water intake, however, pirenzepine produced no effect. The results suggest that M1 and M2 muscarinic receptors activate central pathways involved in the control of water and sodium intake that are under the influence of the LPBN inhibitory mechanisms.


Assuntos
Ingestão de Líquidos/efeitos dos fármacos , Núcleos Parabraquiais/metabolismo , Receptor Muscarínico M1/metabolismo , Receptor Muscarínico M2/metabolismo , Cloreto de Sódio/metabolismo , Animais , Diaminas/farmacologia , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Imidazóis/farmacologia , Masculino , Agonistas Muscarínicos/farmacologia , Antagonistas Muscarínicos/farmacologia , Muscimol/farmacologia , Núcleos Parabraquiais/efeitos dos fármacos , Pilocarpina/farmacologia , Pirenzepina/farmacologia , Ratos , Ratos Sprague-Dawley , Receptor Muscarínico M1/efeitos dos fármacos , Receptor Muscarínico M2/efeitos dos fármacos , Sódio na Dieta
4.
Brain Res Bull ; 139: 174-181, 2018 05.
Artigo em Inglês | MEDLINE | ID: mdl-29432796

RESUMO

The activation of GABA, opioid or α2 adrenergic mechanisms in the lateral parabrachial nucleus (LPBN) facilitates hypertonic NaCl intake in rats. In the present study, we combined opioid or α2 adrenergic antagonists with GABA agonists into the LPBN in order to investigate if NaCl intake caused by GABAergic activation in normohydrated rats depends on opioid or α2-adrenergic mechanisms in this area. Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN were used. Bilateral injections of muscimol or baclofen (GABAA and GABAB agonists, respectively, 0.5 nmol/0.2 µl) into the LPBN induced strong ingestion of 0.3 M NaCl (45.8 ±â€¯7.3 and 21.8 ±â€¯4.8 ml/240 min, respectively) and water intake (22.7 ±â€¯3.4 and 6.6 ±â€¯2.5 ml/240 min, respectively). Naloxone (opioid antagonist, 150 nmol/0.2 µl) into the LPBN abolished 0.3 M NaCl and water intake to muscimol (2.0 ±â€¯0.6 and 0.9 ±â€¯0.2 ml/240 min, respectively) or baclofen (2.3 ±â€¯1.1 and 0.8 ±â€¯0.4 ml/240 min, respectively). RX 821002 (α2 adrenoceptor antagonist, 10 nmol/0.2 µl) into the LPBN reduced 0.3 M NaCl intake induced by the injections of muscimol or baclofen (26.6 ±â€¯8.0 and 10.1 ±â€¯4.9 ml/240 min, respectively). RX 821002 reduced water intake induced by muscimol (7.7 ±â€¯2.9 ml/240 min), not by baclofen. The results suggest that sodium intake caused by gabaergic activation in the LPBN in normohydrated rats is totally dependent on the activation of opioid mechanisms and partially dependent on the activation of α2 adrenergic mechanisms in the LPBN.


Assuntos
Analgésicos Opioides/metabolismo , Agonistas GABAérgicos/farmacologia , Núcleos Parabraquiais/efeitos dos fármacos , Receptores Adrenérgicos alfa 2/metabolismo , Sódio/metabolismo , Antagonistas Adrenérgicos alfa/farmacologia , Animais , Baclofeno/farmacologia , Ingestão de Líquidos/efeitos dos fármacos , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Interações Medicamentosas , Idazoxano/análogos & derivados , Idazoxano/farmacologia , Masculino , Muscimol/farmacologia , Naloxona/farmacologia , Antagonistas de Entorpecentes/farmacologia , Ratos , Fatores de Tempo
5.
Peptides ; 101: 82-88, 2018 03.
Artigo em Inglês | MEDLINE | ID: mdl-29305157

RESUMO

Renovascular hypertensive 2-kidney, 1-clip (2K1C) rats have an increased activity of the renin-angiotensin system and an initial transitory increase in daily water and NaCl intake. However, the dipsogenic and natriorexigenic responses to angiotensin II (ANG II) have not been tested yet in 2K1C rats. Therefore, in the present study, we evaluated water and 0.3 M NaCl intake induced by water deprivation (WD)-partial rehydration (PR) or intracerebroventricular (icv) ANG II in 2K1C rats. In addition, the cardiovascular changes to these treatments were also evaluated. Male Holtzman rats received a silver clip around the left renal artery to induce 2K1C renovascular hypertension. In the 5th week, a group of animals received a guide cannula in the lateral ventricle for icv injections. Daily water intake increased from the 3rd week after surgery and remained elevated until the 6th week (last recording week), whereas daily 0.3 M NaCl intake transiently increased from the 2nd to the 5th week after surgery. On the 6th week, in spite of comparable daily 0.3 M NaCl intake between 2K1C and sham rats, WD-PR and icv ANG II induced an increased 0.3 M NaCl intake in 2K1C rats. Water intake induced by WD-PR, not by icv ANG II, also increased in 2K1C rats. The increase in arterial pressure to WD-PR or icv ANG II was similar in sham and 2K1C rats. Therefore, these results suggest that 2K1C rats are more responsive to the natriorexigenic effects of ANG II, whereas other responses to ANG II are not modified.


Assuntos
Angiotensina II/farmacologia , Apetite/efeitos dos fármacos , Hipertensão Renal/metabolismo , Cloreto de Sódio na Dieta/metabolismo , Sódio/metabolismo , Equilíbrio Hidroeletrolítico/efeitos dos fármacos , Animais , Hipertensão Renal/fisiopatologia , Masculino , Ratos , Ratos Sprague-Dawley
6.
Behav Brain Res ; 333: 17-26, 2017 08 30.
Artigo em Inglês | MEDLINE | ID: mdl-28625546

RESUMO

Angiotensin II (ANG II) is a typical facilitatory stimulus for sodium appetite. Surprisingly, hyperosmolarity and central cholinergic stimulation, two classical antinatriorexigenic stimuli, also facilitate NaCl intake when they are combined with injections of the α2-adrenoceptor/imidazoline agonist moxonidine into the lateral parabrachial nucleus (LPBN). In the present study, we tested the relative importance of central angiotensinergic and cholinergic mechanisms for the control of water and NaCl intake by combining different dipsogenic or natriorexigenic stimuli with moxonidine injection into the LPBN. Adult male Holtzman rats (n=9-10/group) with stainless steel cannulas implanted in the lateral ventricle and LPBN were used. Bilateral injections of moxonidine (0.5 nmol) into the LPBN increased water and 0.3M NaCl intake in rats that received furosemide+captopril injected subcutaneously, ANG II (50ng) or carbachol (cholinergic agonist, 4 nmol) injected intracerebroventricularly (icv) or 2M NaCl infused intragastrically (2ml/rat). Losartan (AT1 antagonist, 100µg) or atropine (muscarinic antagonist, 20 nmol) injected icv abolished the effects on water and 0.3M NaCl of moxonidine combined to either 2M NaCl intragastrically or carbachol icv. However, atropine icv did not change 0.3M NaCl intake produced by direct central action of ANG II like that induced by ANG II icv or furosemide+captopril combined with moxonidine into the LPBN. The results suggest that different stimuli, including hyperosmolarity and central cholinergic stimulation, share central angiotensinergic activation as a common mechanism to facilitate sodium intake, particularly when they are combined with deactivation of the LPBN inhibitory mechanisms.


Assuntos
Inibidores da Enzima Conversora de Angiotensina/farmacologia , Núcleos Parabraquiais/efeitos dos fármacos , Núcleos Parabraquiais/fisiologia , Cloreto de Sódio/metabolismo , Animais , Anti-Hipertensivos/farmacologia , Atropina/farmacologia , Captopril/farmacologia , Ingestão de Líquidos/efeitos dos fármacos , Ingestão de Líquidos/fisiologia , Ingestão de Alimentos/efeitos dos fármacos , Furosemida/farmacologia , Imidazóis/farmacologia , Losartan/farmacologia , Masculino , Antagonistas Muscarínicos/farmacologia , Ratos , Ratos Sprague-Dawley , Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia , Fatores de Tempo
7.
Behav Brain Res ; 316: 11-17, 2017 01 01.
Artigo em Inglês | MEDLINE | ID: mdl-27544874

RESUMO

Facilitatory and inhibitory mechanisms in the central nucleus of the amygdala (CeA) and the lateral parabrachial nucleus (LPBN), respectively, are important for the control of sodium and water intake. Here we investigated the importance of the opioid mechanisms in the CeA for water and 0.3M NaCl intake in euhydrated or hyperosmotic rats treated with injections of muscimol (GABAA agonist) or moxonidine (α2 adrenergic/imidazoline agonist) into the LPBN, respectively. Male Holtzman rats (n=4-8/group) with stainless steel cannulas implanted bilaterally in the CeA and in the LPBN were used. The ingestion of 0.3M NaCl and water by euhydrated rats treated with muscimol (0.5nmol/0.2µl) into the LPBN (29.4±2.7 and 15.0±2.4ml/4h, respectively) was abolished by the previous injections of naloxone (opioid antagonist, 40µg/0.2µl) into the CeA (0.7±0.3 and 0.3±0.1ml/4h, respectively). The ingestion of 0.3M NaCl by rats treated with intragastric 2M NaCl (2ml/rat) combined with moxonidine (0.5nmol/0.2µl) into the LPBN (17.0±3.8ml/2h) was also strongly reduced by the previous injections of naloxone into the CeA (3.2±2.5ml/2h). Sucrose intake was not affected by naloxone injections into the CeA, which minimized the possibility of non-specific inhibition of ingestive behaviors with this treatment. The present results suggest that opioid mechanisms in the CeA are essential for hypertonic NaCl intake when the LPBN inhibitory mechanisms are deactivated or attenuated with injections of muscimol or moxonidine in this area.


Assuntos
Analgésicos Opioides/metabolismo , Núcleo Central da Amígdala/fisiologia , Vias Neurais/fisiologia , Núcleos Parabraquiais/fisiologia , Sódio/metabolismo , Animais , Anti-Hipertensivos/farmacologia , Núcleo Central da Amígdala/efeitos dos fármacos , Ingestão de Líquidos/efeitos dos fármacos , Ingestão de Líquidos/fisiologia , Agonistas de Receptores de GABA-A/farmacologia , Imidazóis/farmacologia , Masculino , Muscimol/farmacologia , Naloxona/farmacologia , Antagonistas de Entorpecentes/farmacologia , Vias Neurais/efeitos dos fármacos , Núcleos Parabraquiais/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Sódio na Dieta
8.
Appetite ; 107: 79-85, 2016 Dec 01.
Artigo em Inglês | MEDLINE | ID: mdl-27460937

RESUMO

History of sodium depletion cross-sensitizes the effects of drugs of abuse. The objective of the present study was to find out if history of sodium depletion also cross-sensitizes a natural reward such as sugar intake in the rat. Sodium depletion was induced by furosemide combined with removal of ambient sodium for 24 h; it was repeated seven days later. The depletion was immediately followed by 0.3 M NaCl intake in a sodium appetite test (active sodium repletion). Seven days after the last depletion, hydrated and fed (need-free) sucrose-naïve animals were offered 10% sucrose in a first 2-h sucrose test. The sucrose test was repeated once a day in a series of five consecutive days. History of sodium depletion enhanced sucrose intake in the first and second tests; it had no effect from the third to fifth sucrose test. The effect on the initial sucrose intake tests disappeared if the rats did not ingest 0.3 M NaCl in the sodium appetite test. Prior experience with sucrose intake in need-free conditions had no effect on sodium appetite. History of intracellular dehydration transiently influenced sucrose intake in the first sucrose test. We found no evidence for thirst sensitization. We conclude that history of dehydration, particularly that resulting from sodium depletion, combined to active sodium repletion, produced short-term cross-sensitization of sucrose intake in sucrose-naïve rats. The results suggest that the cross-sensitization of sucrose intake related with acquisition of sugar as a novel nutrient rather than production of lasting effects on sugar rewarding properties.


Assuntos
Dieta Hipossódica , Açúcares da Dieta/administração & dosagem , Cloreto de Sódio na Dieta/administração & dosagem , Sódio na Dieta/administração & dosagem , Animais , Apetite , Desidratação , Furosemida/administração & dosagem , Masculino , Ratos , Ratos Sprague-Dawley , Sede
9.
Am J Physiol Regul Integr Comp Physiol ; 310(1): R15-23, 2016 Jan 01.
Artigo em Inglês | MEDLINE | ID: mdl-26538239

RESUMO

iSodium intake occurs either as a spontaneous or induced behavior, which is enhanced, i.e., sensitized, by repeated episodes of water deprivation followed by subsequent partial rehydration (WD-PR). In the present work, we examined whether repeated WD-PR alters hypothalamic transcripts related to the brain renin-angiotensin system (RAS) and apelin system in male normotensive Holtzman rats (HTZ). We also examined whether the sodium intake of a strain with genetically inherited high expression of the brain RAS, the spontaneously hypertensive rat (SHR), responds differently than HTZ to repeated WD-PR. We found that repeated WD-PR, besides enhancing spontaneous and induced 0.3 M NaCl intake, increased the hypothalamic expression of angiotensinogen, aminopeptidase N, and apelin receptor transcripts (43%, 60%, and 159%, respectively) in HTZ at the end of the third WD-PR. Repeated WD-PR did not change the daily spontaneous 0.3 M NaCl intake and barely changed the need-induced 0.3 M NaCl intake of SHR. The same treatment consistently enhanced spontaneous daily 0.3 M NaCl intake in the normotensive Wistar-Kyoto rats. The results show that repeated WD-PR produces alterations in hypothalamic transcripts and also sensitizes sodium appetite in HTZ. They suggest an association between the components of hypothalamic RAS and the apelin system, with neural and behavioral plasticity produced by repeated episodes of WD-PR in a normotensive strain. The results also indicate that the inherited hyperactive brain RAS is not a guarantee for sensitization of sodium intake in the male adult SHR exposed to repeated WD-PR.


Assuntos
Regulação do Apetite , Comportamento Animal , Hidratação , Hipertensão/metabolismo , Hipotálamo/metabolismo , Peptídeos e Proteínas de Sinalização Intercelular/metabolismo , RNA Mensageiro/metabolismo , Sistema Renina-Angiotensina , Cloreto de Sódio na Dieta/administração & dosagem , Privação de Água , Animais , Apelina , Modelos Animais de Doenças , Regulação da Expressão Gênica , Hipertensão/genética , Hipertensão/fisiopatologia , Hipertensão/psicologia , Peptídeos e Proteínas de Sinalização Intercelular/genética , Masculino , Plasticidade Neuronal , RNA Mensageiro/genética , Ratos Endogâmicos SHR , Ratos Endogâmicos WKY , Ratos Sprague-Dawley , Sistema Renina-Angiotensina/genética , Fatores de Tempo
10.
J Physiol ; 594(6): 1607-16, 2016 Mar 15.
Artigo em Inglês | MEDLINE | ID: mdl-26036817

RESUMO

Sickness behaviour, a syndrome characterized by a general reduction in animal activity, is part of the active-phase response to fight infection. Lipopolysaccharide (LPS), an effective endotoxin to model sickness behaviour, reduces thirst and sodium excretion, and increases neurohypophysial secretion. Here we review the effects of LPS on thirst and sodium appetite. Altered renal function and hydromineral fluid intake in response to LPS occur in the context of behavioural reorganization, which manifests itself as part of the syndrome. Recent data show that, in addition to its classical effect on thirst, non-septic doses of LPS injected intraperitoneally produce a preferential inhibition of intracellular thirst versus extracellular thirst. Moreover, LPS also reduced hypertonic NaCl intake in sodium-depleted rats that entered a sodium appetite test. Antagonism of α2 -adrenoceptors abolished the effect of LPS on sodium appetite. LPS and cytokine transduction potentially recruit brain noradrenaline and α2 -adrenoceptors to control sodium appetite and sickness behaviour.


Assuntos
Apetite , Comportamento de Doença , Receptores Adrenérgicos alfa 2/metabolismo , Sódio/metabolismo , Animais , Lipopolissacarídeos/toxicidade , Equilíbrio Hidroeletrolítico
11.
Brain Res ; 1625: 238-45, 2015 Nov 02.
Artigo em Inglês | MEDLINE | ID: mdl-26358148

RESUMO

The lateral parabrachial nucleus (LPBN) and the central nucleus of the amygdala (CeA) are important central areas for the control of sodium appetite. In the present study, we investigated the importance of the facilitatory mechanisms of the CeA on NaCl and water intake produced by the deactivation of LPBN inhibitory mechanisms. Male Holtzman rats (n=7-14) with stainless steel cannulas implanted bilaterally in the CeA and LPBN were used. Bilateral injections of moxonidine (α2-adrenoceptor/imidazoline agonist, 0.5 nmol/0.2 µl) into the LPBN increased furosemide+captopril-induced 0.3M NaCl (29.7 ± 7.2, vs. vehicle: 4.4 ± 1.6 ml/2h) and water intake (26.4 ± 6.7, vs. vehicle: 8.2 ± 1.6 ml/2h). The GABAA agonist muscimol (0.25 nmol/0.2 µl) injected bilaterally into the CeA abolished the effects of moxonidine into the LPBN on 0.3M NaCl (2.8 ± 1.6 ml/2h) and water intake (3.3 ± 2.3 ml/2h). Euhydrated rats treated with muscimol (0.5 nmol/0.2 µl) into the LPBN also ingested 0.3M NaCl (19.1 ± 6.4 ml/4h) and water (8.8 ± 3.2 ml/4h). Muscimol (0.5 nmol/0.2 µl) into the CeA also abolished 0.3M NaCl (0.1 ± 0.04 ml/4h) and water intake (0.1 ± 0.02 ml/4h) in euhydrated treated with muscimol into the LPBN. The present results show that neuronal deactivation of the CeA abolishes NaCl intake produced by the blockade of LPBN inhibitory mechanisms, suggesting an interaction between facilitatory mechanisms of the CeA and inhibitory mechanisms of the LPBN in the control of NaCl intake.


Assuntos
Núcleo Central da Amígdala/fisiologia , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Núcleos Parabraquiais/fisiologia , Sódio/metabolismo , Animais , Anti-Hipertensivos/farmacologia , Captopril/farmacologia , Núcleo Central da Amígdala/efeitos dos fármacos , Ingestão de Líquidos/efeitos dos fármacos , Furosemida/farmacologia , Agonistas de Receptores de GABA-A/farmacologia , Imidazóis/farmacologia , Masculino , Muscimol/farmacologia , Vias Neurais/efeitos dos fármacos , Vias Neurais/fisiologia , Ratos , Ratos Sprague-Dawley , Inibidores de Simportadores de Cloreto de Sódio e Potássio/farmacologia , Fatores de Tempo
12.
Physiol Behav ; 151: 494-501, 2015 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-26297688

RESUMO

Water deprivation (WD) followed by water intake to satiety, produces satiation of thirst and partial rehydration (PR). Thus, WD-PR is a natural method to differentiate thirst from sodium appetite. WD-PR also produces Fos immunoreactivity (Fos-ir) in interconnected areas of a brain circuit postulated to subserve sodium appetite. In the present work, we evaluated the effect of sodium intake on Fos-ir produced by WD-PR in brain areas operationally defined according to the literature as either facilitatory or inhibitory to sodium intake. Isotonic NaCl was available for ingestion in a sodium appetite test performed immediately after a single episode of WD-PR. Sodium intake decreased Fos-ir in facilitatory areas such as the lamina terminalis (particularly subfornical organ and median preoptic nucleus), central amygdala and hypothalamic parvocellular paraventricular nucleus in the forebrain. Sodium intake also decreased Fos-ir in inhibitory areas such as the area postrema, lateral parabrachial nucleus and nucleus of the solitary tract in the hindbrain. In contrast, sodium intake further increased Fos-ir that was activated by water deprivation in the dorsal raphe nucleus, another inhibitory area localized in the hindbrain. WD-PR increased Fos-ir in the core and shell of the nucleus accumbens. Sodium intake reduced Fos-ir in both parts of the accumbens. In summary, sodium intake following WD-PR reduced Fos-ir in most facilitatory and inhibitory areas, but increased Fos-ir in another inhibitory area. It also reduced Fos-ir in a reward area (accumbens). The results suggest a functional link between sodium intake and the activity of the hindbrain-forebrain circuitry subserving reward and sodium appetite in response to water deprivation.


Assuntos
Encéfalo/metabolismo , Desidratação/metabolismo , Desidratação/terapia , Hidratação , Proteínas Proto-Oncogênicas c-fos/metabolismo , Privação de Água/fisiologia , Animais , Apetite/fisiologia , Encéfalo/patologia , Desidratação/patologia , Ingestão de Líquidos/fisiologia , Hidratação/métodos , Masculino , Fotomicrografia , Ratos Wistar , Recompensa , Cloreto de Sódio na Dieta/administração & dosagem , Sede/fisiologia
13.
Physiol Behav ; 151: 111-20, 2015 Nov 01.
Artigo em Inglês | MEDLINE | ID: mdl-26171591

RESUMO

Previous studies from our laboratory have shown that methysergide, a serotonergic antagonist, injected into the lateral parabrachial nucleus (LPBN) combined with a pre-load of 2 M NaCl, given by gavage, induces 0.3 M NaCl intake. The mechanisms involved in this paradoxical behavior are still unknown. In the present work, we investigated the effect of serotonergic blockade into the LPBN on hindbrain and hypothalamic activity, gastric emptying and arterial blood pressure in cell-dehydrated rats. Methysergide plus 2 M NaCl infused intragastrically or intravenously promoted 0.3 M NaCl intake in two-bottle tests. In cell-dehydrated rats with no access to fluids, methysergide compared to vehicle increased Fos immunoreactivity in the medial nucleus of the solitary tract, area postrema and non-oxytocinergic cells of the ventral portion of the hypothalamic paraventricular nucleus (PVN). There was no alteration in the number of neurons double-labeled for Fos-ir and oxytocin in the PVN and supraoptic nuclei. There was also no alteration in plasma oxytocin and vasopressin, or arterial pressure. In rats cell-dehydrated by i.v. 2 M NaCl, methysergide also did not change the amount of an intragastric load of 0.3 M NaCl retained in the stomach or intestine. The results suggest that methysergide injected into the LPBN of cell-dehydrated rat does not alter primary inhibitory signals that control sodium intake. The inhibitory signals blocked by methysergide in the LPBN possibly originated from activation of brain osmoreceptors, second order visceral/hormonal signals or a combination of both.


Assuntos
Desidratação/metabolismo , Esvaziamento Gástrico/efeitos dos fármacos , Metisergida/farmacologia , Núcleos Parabraquiais/efeitos dos fármacos , Solução Salina Hipertônica , Antagonistas da Serotonina/farmacologia , Animais , Área Postrema/efeitos dos fármacos , Área Postrema/metabolismo , Pressão Arterial/efeitos dos fármacos , Pressão Arterial/fisiologia , Modelos Animais de Doenças , Esvaziamento Gástrico/fisiologia , Masculino , Neurônios/efeitos dos fármacos , Neurônios/metabolismo , Ocitocina/metabolismo , Núcleos Parabraquiais/metabolismo , Proteínas Proto-Oncogênicas c-fos/metabolismo , Ratos Sprague-Dawley , Solução Salina Hipertônica/administração & dosagem , Cloreto de Sódio na Dieta/administração & dosagem , Núcleo Solitário/efeitos dos fármacos , Núcleo Solitário/metabolismo , Núcleo Supraóptico/efeitos dos fármacos , Núcleo Supraóptico/metabolismo , Vasopressinas/sangue
14.
Behav Brain Res ; 288: 20-5, 2015 Jul 15.
Artigo em Inglês | MEDLINE | ID: mdl-25827924

RESUMO

Important inhibitory mechanisms for the control of water and sodium intake are present in the lateral parabrachial nucleus (LPBN). Opioid receptors are expressed by LPBN neurons and injections of ß-endorphin (nonspecific opioid receptor agonist) in this area induce 0.3M NaCl and water intake in satiated rats. In the present study, we investigated the effects of the injections of endomorphin-1 (µ opioid receptor agonist) alone or combined with the blockade of µ, κ or δ opioid receptors into the LPBN on 0.3M NaCl and water intake induced by subcutaneous injections of the diuretic furosemide (FURO) combined with low dose of the angiotensin converting enzyme inhibitor captopril (CAP). Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN were used. Bilateral injections of endomorphin-1 (0.1, 0.25, 0.5, 1.0, 2.0 and 4.0nmol/0.2µl) into the LPBN increased 0.3M NaCl and water intake induced by FURO+CAP. The previous blockade of µ opioid receptor with CTAP (1.0nmol/0.2µl) into the LPBN reduced the effect of endomorphin-1 on FURO+CAP-induced 0.3M NaCl. GNTI (κ opioid receptor antagonist; 2.0nmol/0.2µl) and naltrindole (δ opioid receptor antagonist; 2.0nmol/0.2µl) injected into the LPBN did not change the effects of endomorphin-1 on FURO+CAP-induced 0.3M NaCl. The results suggest that µ opioid receptors in the LPBN are involved in the control of sodium intake.


Assuntos
Regulação do Apetite/fisiologia , Ingestão de Líquidos/fisiologia , Núcleos Parabraquiais/metabolismo , Receptores Opioides mu/metabolismo , Sódio na Dieta , Analgésicos Opioides/farmacologia , Inibidores da Enzima Conversora de Angiotensina/farmacologia , Animais , Regulação do Apetite/efeitos dos fármacos , Diuréticos/farmacologia , Relação Dose-Resposta a Droga , Ingestão de Líquidos/efeitos dos fármacos , Água Potável , Masculino , Antagonistas de Entorpecentes/farmacologia , Oligopeptídeos/farmacologia , Núcleos Parabraquiais/efeitos dos fármacos , Ratos Sprague-Dawley , Receptores Opioides delta/antagonistas & inibidores , Receptores Opioides delta/metabolismo , Receptores Opioides kappa/antagonistas & inibidores , Receptores Opioides kappa/metabolismo , Receptores Opioides mu/agonistas , Receptores Opioides mu/antagonistas & inibidores , Cloreto de Sódio
15.
Am J Physiol Regul Integr Comp Physiol ; 306(4): R201-10, 2014 Feb 15.
Artigo em Inglês | MEDLINE | ID: mdl-24401989

RESUMO

In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review.


Assuntos
Apetite/fisiologia , Rombencéfalo/fisiologia , Sódio na Dieta , Animais , Inibição Neural , Vias Neurais/fisiologia , Prosencéfalo/fisiologia , Equilíbrio Hidroeletrolítico
16.
Neurosci Lett ; 556: 32-6, 2013 Nov 27.
Artigo em Inglês | MEDLINE | ID: mdl-24095671

RESUMO

Injection of l-glutamate (GLU) into the rostral ventrolateral medulla (RVLM) produces sympathetically-mediated pressor responses that depend on the integrity of the tissue surrounding the anteroventral third ventricle (AV3V region). The injection of angiotensin II (ANG II) or the cholinergic agonist carbachol into the RVLM also produces pressor responses. In the present study, we investigated if the lesion of the AV3V region affects the pressor responses to ANG II or carbachol injected into the RVLM in unanesthetized rats. Male Holtzman rats with sham or electrolytic AV3V lesions and a stainless steel cannula implanted into the RVLM were used. The pressor responses to ANG II (200ng/100nl) injected into the RVLM were reduced by acute (1 day) (12±3 vs. sham lesions: 26±4mmHg) or chronic (15 days) AV3V lesions (12±5 vs. sham lesions: 27±4mmHg), whereas acute or chronic AV3V lesions did not affect the pressor responses to carbachol (1nmol/100nl) injected into the RVLM. The present results suggest that the AV3V region modulates the excitability of the RVLM neurons involved with the pressor response produced by the activation of angiotensinergic mechanisms in this area.


Assuntos
Angiotensina II/farmacologia , Pressão Sanguínea/efeitos dos fármacos , Carbacol/farmacologia , Ventrículos Cerebrais/fisiologia , Agonistas Colinérgicos/farmacologia , Frequência Cardíaca/efeitos dos fármacos , Bulbo , Angiotensina II/administração & dosagem , Animais , Carbacol/administração & dosagem , Agonistas Colinérgicos/administração & dosagem , Eletrólise , Masculino , Ratos , Ratos Sprague-Dawley
17.
Neurosci Lett ; 534: 188-92, 2013 Feb 08.
Artigo em Inglês | MEDLINE | ID: mdl-23219800

RESUMO

Bilateral injections of the GABA(A) agonist muscimol into the lateral parabrachial nucleus (LPBN) disrupt satiety and induce strong ingestion of water and 0.3M NaCl in fluid-replete rats by mechanisms not completely clear. In the present study, we investigated the effects of the blockade of central muscarinic cholinergic receptors with atropine injected intracerebroventricularly (i.c.v.) on 0.3M NaCl and water intake induced by muscimol injections into the LPBN in fluid-replete rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally into the LPBN and unilaterally into the lateral ventricle (LV) were used. Bilateral injections of muscimol (0.5nmol/0.2µL) into the LPBN induced 0.3M NaCl (32.2±9.9mL/4h, vs. saline: 0.4±0.2mL/4h) and water intake (11.4±4.4mL/4h, vs. saline: 0.8±0.4mL/4h) in fluid-replete rats previously treated with i.c.v. injection of saline. The previous i.c.v. injection of atropine (20nmol/1µL) reduced the effects of LPBN-muscimol on 0.3M NaCl (13.5±5.0mL/4h) and water intake (2.9±1.6mL/4h). The i.c.v. injection of atropine did not affect 0.3M NaCl (26.8±6.2mL/2h, vs. saline i.c.v.: 36.5±9.8mL/2h) or water intake (14.4±2.5mL/2h, vs. saline i.c.v.: 15.6±4.8mL/2h) in rats treated with furosemide+captopril subcutaneously combined with bilateral injections of moxonidine (α(2)-adrenoceptor/imidazoline agonist, 0.5nmol/0.2µL) into the LPBN, suggesting that the effect of atropine was not due to non-specific inhibition of ingestive behaviors. The results show that active central cholinergic mechanisms are necessary for the hypertonic NaCl and water intake induced by the blockade of the inhibitory mechanisms with injections of muscimol into the LPBN in fluid-replete rats. The suggestion is that in fluid-replete rats the action of LPBN mechanisms inhibits facilitatory signals produced by the activity of central cholinergic mechanisms to maintain satiety.


Assuntos
Ingestão de Alimentos/fisiologia , Ponte/metabolismo , Receptores de GABA-A/metabolismo , Receptores Muscarínicos/metabolismo , Cloreto de Sódio/metabolismo , Antagonistas de Receptores de Angiotensina/farmacologia , Inibidores da Enzima Conversora de Angiotensina/farmacologia , Animais , Atropina/farmacologia , Captopril/farmacologia , Diuréticos/farmacologia , Ingestão de Líquidos/efeitos dos fármacos , Ingestão de Alimentos/efeitos dos fármacos , Furosemida/farmacologia , Agonistas GABAérgicos/farmacologia , Imidazóis/farmacologia , Injeções Intraventriculares , Losartan/farmacologia , Masculino , Antagonistas Muscarínicos/farmacologia , Muscimol/farmacologia , Ponte/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley
18.
Neurosci Lett ; 521(1): 31-6, 2012 Jul 11.
Artigo em Inglês | MEDLINE | ID: mdl-22634629

RESUMO

Electrolytic lesions of the commissural nucleus of the solitary tract (commNTS) in rats enhance the pressor response to bilateral carotid occlusion or to intravenous infusion of hypertonic NaCl without changing baroreflex responses. In an opposite direction, commNTS lesions abolish the pressor responses to peripheral chemoreflex activation. These opposite effects of commNTS lesions apparently result from an impairment of sympathetic activation in one case and in a facilitation of vasopressin secretion in the others. In the present study, we investigated the effects of the electrolytic lesions of the commNTS in the pressor responses that depend on sympathetic activation and vasopressin secretion produced by central cholinergic or adrenergic activation with intracerebroventricular (i.c.v.) injections of carbachol or noradrenaline, respectively, in unanesthetized rats. Male Holtzman rats (280-320 g, n=8-15/group) with acute (1 day) or chronic (21 days) sham or commNTS lesions (1 mA×10 s) and a stainless steel cannula implanted in the lateral ventricle were used. Acute commNTS lesions increased the pressor response to i.c.v. injection of carbachol (0.5 nmol/1µ1) (52 ± 2, vs. sham: 37 ± 2mm Hg) or noradrenaline (80 nmol/1µl) (45 ± 6, vs. sham: 30 ± 3 mm Hg), whereas chronic commNTS lesions did not affect the pressor responses to the same treatments. Lesions of the commNTS impaired chemoreflex responses produced by intravenous KCN, without changing baroreflex responses. The results suggest that commNTS-dependent inhibitory signals are involved in the modulation of the pressor responses to central cholinergic and adrenergic activation, probably limiting vasopressin secretion.


Assuntos
Agonistas alfa-Adrenérgicos/farmacologia , Carbacol/farmacologia , Agonistas Colinérgicos/farmacologia , Norepinefrina/farmacologia , Núcleo Solitário/fisiopatologia , Animais , Barorreflexo , Células Quimiorreceptoras/fisiologia , Eletrólise , Injeções Intraventriculares , Masculino , Ratos , Ratos Sprague-Dawley , Núcleo Solitário/patologia , Vasopressinas/metabolismo
19.
Physiol Behav ; 104(5): 702-8, 2011 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-21803064

RESUMO

Bilateral injections of moxonidine, an α2-adrenoceptor and imidazoline receptor agonist, into the lateral parabrachial nuclei (LPBN) enhance sodium appetite induced by extracellular dehydration. In the present study, we examined whether LPBN moxonidine treatments change taste reactivity to hypertonic NaCl solution administered into the mouth by intra-oral (IO) cannula. Male Holtzman rats prepared with IO and bilateral LPBN cannulas received subcutaneous injections of furosemide (FURO; 10 mg/kg) and captopril (CAP; 5 mg/kg) to induce hypovolemia with mild hypotension and an accompanying salt appetite and thirst before testing the taste reactivity to oral infusions of 0.3 M NaCl (1.0 ml/min). In the first experiment 45 min after subcutaneous injections of FURO+CAP or vehicle, moxonidine was bilaterally injected into the LPBN, and then 15 min later both bodily and oral-facial ingestive and rejection responses to 0.3 M NaCl delivered through the IO cannula were assessed. Both LPBN vehicle and moxonidine treated rats showed increased ingestive and decreased rejection responses to the IO hypertonic solution. The IO 0.3 M NaCl infusion-evoked ingestive and rejection taste related behaviors were comparable in the LPBN vehicle- vs. the LPBN moxonidine-injected groups. In a second experiment, rats received the same FURO+CAP treatments and LPBN injections. However, beginning 15 min after the LPBN injections, they were given access to water and 0.3M NaCl and were allowed to consume the fluids for most of the next 60 min with the free access intake being interrupted only for a few minutes at 15, 30 and 60 min after the fluids became available. During each of these three brief periods, a taste reactivity test was conducted. On the three taste reactivity tests rats that received LPBN vehicle injections showed progressive declines in ingestive responses and gradual increases in rejection responses. However, in contrast to the LPBN vehicle treated rats, animals receiving bilateral injections of LPBN moxonidine maintained a high number of ingestive responses and a low number of rejection responses throughout the test period even in spite of evidencing substantial water and 0.3 M NaCl consumption during the periods of free access. The results suggest that after α2-adrenoceptor agonist delivery to the LPBN the acceptance of 0.3 M NaCl is sustained and the negative attributes of the solution are minimized. The maintained positive rewarding qualities of 0.3 M NaCl are likely to account for why LPBN moxonidine treated rats show such a remarkable salt appetite when assayed by the volume of hypertonic 0.3 M NaCl consumed.


Assuntos
Agonistas Adrenérgicos/farmacologia , Imidazóis/farmacologia , Ponte/efeitos dos fármacos , Solução Salina Hipertônica/administração & dosagem , Paladar/efeitos dos fármacos , Animais , Anti-Hipertensivos/farmacologia , Captopril/farmacologia , Diuréticos/farmacologia , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Vias de Administração de Medicamentos , Interações Medicamentosas , Furosemida/farmacologia , Masculino , Ponte/fisiologia , Ratos , Fatores de Tempo
20.
Physiol Behav ; 104(5): 659-65, 2011 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-21781982

RESUMO

Gavage of 2 M NaCl (IG 2 M NaCl), a procedure to induce cell-dehydration-and water and 0.15 M NaCl intake in a two-bottle choice test-is also a potential gastric irritant. In this study, we assessed whether mineral intake induced by IG 2 M NaCl is associated with gastric irritation or production of pica in the rat. We first determined the amount of mineral solution (0.15 M NaCl, 0.15 M NaHCO3, 0.01 M KCl and 0.05 mM CaCl2) and water ingested in response to IG 2 M NaCl in a five-bottle test. Then, we used mineral solutions (0.01 M KCl and 0.15 M NaHCO3), whose intakes were significantly increased compared to controls, and water in three-bottle tests to test the gastric irritation hypothesis. The IG 2 M NaCl induced KCl and NaHCO3 intake that was not inhibited by gavage with gastric protectors Al(OH)3 or NaHCO3. IG 2 M NaCl or gavage of 0.6 N acetic acid induced mild irritation, hyperemia, of the glandular part of the stomach. A gavage of 50% ethanol induced strong irritation seen as pinpoint ulcerations. Neither ethanol nor acetic acid induced any fluid intake. Neither IG 2 M NaCl nor acetic acid induced kaolin intake, a marker of pica in laboratory rats. Ethanol did induce kaolin intake. These results suggest that IG 2 M NaCl induced a mineral fluid intake not selective for sodium and independent from gastric irritation or pica.


Assuntos
Desidratação/complicações , Comportamento de Ingestão de Líquido/fisiologia , Ingestão de Líquidos/fisiologia , Gastrite/etiologia , Águas Minerais , Pica/etiologia , Cloreto de Sódio/administração & dosagem , Ácido Acético/administração & dosagem , Análise de Variância , Animais , Comportamento de Escolha/fisiologia , Ingestão de Líquidos/efeitos dos fármacos , Comportamento de Ingestão de Líquido/efeitos dos fármacos , Etanol/administração & dosagem , Preferências Alimentares/efeitos dos fármacos , Lavagem Gástrica/métodos , Mucosa Gástrica/efeitos dos fármacos , Mucosa Gástrica/patologia , Gastrite/patologia , Masculino , Ratos , Solução Salina Hipertônica/administração & dosagem , Bicarbonato de Sódio/administração & dosagem , Cloreto de Sódio/metabolismo
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