Navegando por Autor "Luca Junior, L. A. de"
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Item Baclofen into the lateral parabrachial nucleus induces hypertonic sodium chloride and sucrose intake in rats.(2011) Oliveira, Lisandra Brandino de; Kimura, Everton Heidi; Callera, João Carlos; Luca Junior, L. A. de; Colombari, Débora Simões de AlmeidaGABAA and GABAB receptors are present in the lateral parabrachial nucleus (LPBN), a pontine area involved with inhibitory mechanisms related to the control of sodium appetite. Activation of GABAA receptors in the LPBN induces strong ingestion of 0.3 M sodium chloride (NaCl) in normonatremic and euhydrated rats. In the present study, we investigated the effects of the GABAB receptor agonist baclofen, injected alone or combined with GABAA or GABAB receptor antagonists into the LPBN on 0.3 M NaCl, water, 0.06 M sucrose and food intake in normonatremic and euhydrated rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN were used. In normonatremic and euhydrated rats, bilateral injections of baclofen (0.5 nmol/0.2 _l) into the LPBN induced 0.3 M NaCl (24.0_3.1 vs. saline: 2.0_0.8 ml/240 min) and water intake (10.6_1.4 vs. saline: 3.5_0.7 ml/240 min) in a two-bottle test. Injections of GABAB receptor antagonists CGP 35348 (50 nmol/0.2 _l) or 2-hydroxysaclofen (5 nmol/0.2 _l) or GABAA receptor antagonist bicuculline (1.6 nmol/0.2 _l) into the LPBN reduced 0.3 M NaCl (14.1_4.7 ml/240 min; 9.97_2.5 ml/210 min; 8.8_5.9 ml/240 min, respectively) and water intake induced by baclofen injected into the LPBN. Baclofen (0.5 nmol/0.2 _l) injected into the LPBN also induced 0.06 M sucrose intake (21.8_5.9 vs. saline: 5.0_2.6 ml/180 min). Urinary volume and sodium excretion had a tendency to decrease after baclofen injection into the LPBN, whereas arterial pressure and food intake were not affected. The results show that baclofen injected into the LPBN, in normonatremic and euhydrated rats, produces a natriorexigenic effect dependent on GABAA and GABAB receptor activation. The natriorexigenic effect is not secondary to alterations in blood pressure or sodium urinary excretion. In addition, baclofen injected into the LPBN also induces 0.06 M sucrose intake.Item GABAergic mechanisms of the lateral parabrachial nucleus on sodium appetite.(2007) Oliveira, Lisandra Brandino de; Callera, João Carlos; Luca Junior, L. A. de; Colombari, Débora Simões de Almeida; Menani, José VanderleiGABAergic activation in the lateral parabrachial nucleus (LPBN) induces sodium and water intake in satiated and normovolemic rats. In the present study we investigated the effects of GABAA receptor activation in the LPBN on 0.3M NaCl, water, 2% sucrose and food intake in rats submitted to sodium depletion (treatment with the diuretic furosemide subcutaneously + sodium deficient food for 24 h), 24 h food deprivation or 24 h water deprivation. Male Holtzman rats with bilateral stainless steel cannulas implanted into the LPBN were used. In sodium depleted rats, muscimol (GABAA receptor agonist, 0.5 nmol/0.2 _l), bilaterally injected into the LPBN, produced an inconsistent increase of water intake and two opposite effects on 0.3M NaCl intake: an early inhibition (4.3±2.7 versus saline: 14.4±1.0 ml/15 min) and a late facilitation (37.6±2.7 versus saline: 21.1±0.9 ml/180 min). The pretreatment of the LPBN with bicuculline (GABAA receptor antagonist, 1.6 nmol) abolished these effects of muscimol. Muscimol into the LPBN also reduced food deprivation-induced food intake in the first 30 min of test (1.7±0.6 g versus saline: 4.1±0.6 g), without changing water deprivation-induced water intake or 2% sucrose intake in sodium depleted rats. Therefore, although GABAA receptors in the LPBN are not tonically involved in the control of sodium depletion-induced sodium intake, GABAA receptor activation in the LPBN produces an early inhibition and a late facilitation of sodium depletion-induced sodium intake. GABAA activation in the LPBN also inhibits food intake, while it consistently increases only sodium intake and not water, food or sucrose intake.Item Inhibition of central angiotensin II-induced pressor responses by hydrogen peroxide.(2010) Lauar, M. R.; Colombari, Débora Simões de Almeida; Paula, Patricia Maria de; Colombari, Eduardo; Cardoso, Leonardo Máximo; Luca Junior, L. A. de; Menani, José VanderleiHydrogen peroxide (H2O2), important reactive oxygen species produced endogenously, may have different physiological actions. The superoxide anion (O2 •_) is suggested to be part of the signaling mechanisms activated by angiotensin II (ANG II) and central virus-mediated overexpression of the enzyme superoxide dismutase (that dismutates O2 •_ to H2O2) reduces pressor and dipsogenic responses to central ANG II. Whether this result might reflect elevation of H2O2 rather than depletion of O2 •_ has not been addressed. Here we investigated the effects of H2O2 injected intracerebroventricularly (i.c.v.) or ATZ (3-amino-1,2,4-triazole, a catalase inhibitor) injected intravenously (i.v.) or i.c.v. on the pressor responses induced by i.c.v. injections of ANG II. Normotensive male Holtzman rats (280–320 g, n_5–13/ group) with stainless steel cannulas implanted in the lateral ventricle were used. Prior injection of H2O2 (5 _mol/1 _l) or ATZ (5 nmol/1 _l) i.c.v. almost abolished the pressor responses induced by ANG II (50 ng/1 _l) also injected i.c.v. (7_3 and 5_3 mm Hg, respectively, vs. control: 19_4 mm Hg). Injection of ATZ (3.6 mmol/kg b.wt.) i.v. also reduced central ANG II-induced pressor responses. Injections of H2O2 i.c.v. and ATZ i.c.v. or i.v. alone produced no effect on baseline arterial pressure. Central ANG II, H2O2 or ATZ did not affect heart rate. The results show that central injections of H2O2 and central or peripheral injections of ATZ reduced the pressor responses induced by i.c.v. ANG II, suggesting that exogenous or endogenous H2O2 may inhibit central pressor mechanisms activated by ANG II.Item Opioid activation in the lateral parabrachial nucleus induces hypertonic sodium intake.(2008) Oliveira, Lisandra Brandino de; Luca Junior, L. A. de; Menani, José VanderleiOpioid mechanisms are involved in the control of water and NaCl intake and opioid receptors are present in the lateral parabrachial nucleus (LPBN), a site of important inhibitory mechanisms related to the control of sodium appetite. Therefore, in the present study we investigated the effects of opioid receptor activation in the LPBN on 0.3 M NaCl and water intake in rats. Male Holtzman rats with stainless steel cannulas implanted bilaterally in the LPBN were used. In normohydrated and satiated rats, bilateral injections of the opioid receptor agonist _-endorphin (2 nmol/0.2 _l) into the LPBN induced 0.3 M NaCl (17.8_5.9 vs. saline: 0.9_0.5 ml/240 min) and water intake (11.4_3.0 vs. saline: 1.0_0.4 ml/240 min) in a two-bottle test. Bilateral injections of the opioid antagonist naloxone (100 nmol/ 0.2 _l) into the LPBN abolished sodium and water intake induced by _-endorphin into the LPBN and also reduced 0.3 M NaCl intake (12.8_1.5 vs. vehicle: 22.4_3.1 ml/180 min) induced by 24 h of sodium depletion (produced by the treatment with the diuretic furosemide s.c._sodium deficient food for 24 h). Bilateral injections of _-endorphin into the LPBN in satiated rats produced no effect on water or 2% sucrose intake when water alone or simultaneously with 2% sucrose was offered to the animals. The results show that opioid receptor activation in the LPBN induces hypertonic sodium intake in satiated and normohydrated rats, an effect not due to general ingestive behavior facilitation. In addition, sodium depletion induced 0.3 M NaCl intake also partially depends on opioid receptor activation in the LPBN. The results suggest that deactivation of inhibitory mechanisms by opioid receptor activation in the LPBN releases sodium intake if excitatory signals were activated (sodium depletion) or not.Item Sodium intake by hyperosmotic rats treated with a GABAA receptor agonist into the lateral parabrachial nucleus.(2008) Kimura, Everton Heidi; Oliveira, Lisandra Brandino de; Colombari, Débora Simões de Almeida; Luca Junior, L. A. de; Menani, José Vanderlei; Callera, João CarlosInhibitory mechanisms in the lateral parabrachial nucleus (LPBN) and central GABAergic mechanisms are involved in the regulation of water and NaCl intake. Besides increasing fluid depletion-induced sodium intake, the activation of GABAA receptors with muscimol into the LPBN also induces ingestion of 0.3 M NaCl in normonatremic, euhydrated rats. It has been suggested that inhibitory mechanisms activated by osmotic signals are blocked by GABAA receptor activation in the LPBN, thereby increasing hypertonic NaCl intake. Therefore, in the present study we investigated the effects of muscimol injected into the LPBN on water and 0.3MNaCl intake in hyperosmotic cell-dehydrated rats (rats treated with an intragastric load of 2 M NaCl). Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. In euhydrated rats, muscimol (0.5 nmol/0.2 μl), bilaterally injected into the LPBN, induced ingestion of 0.3 M NaCl (24.6±7.9 vs. vehicle: 0.5±0.3 ml/180 min) and water (6.3±2.1 vs. vehicle: 0.5±0.3 ml/180 min). One hour after intragastric 2 M NaCl load (2 ml), bilateral injections of muscimol into the LPBN also induced 0.3 M NaCl intake (22.1±5.2 vs. vehicle: 0.9±0.8 ml/210 min) and water intake (16.5±3.6 vs. vehicle: 7.8±1.8 ml/210 min). The GABAA antagonist bicuculline (0.4 nmol/0.2 μl) into the LPBN reduced the effect of muscimol on 0.3MNaCl intake (7.1±2.1 ml/210 min). Therefore, the activation ofGABAA receptors in the LPBN induces ingestion of 0.3 M NaCl by hyperosmotic cell-dehydrated rats, suggesting that plasma levels of renin or osmolarity do not affect sodium intake after the blockade of LPBN inhibitory mechanisms with muscimol.