Navegando por Autor "Kimura, Everton Heidi"
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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 Baclofen into the lateral parabrachial nucleus induces hypertonic sodium chloride intake during cell dehydration.(2013) Kimura, Everton Heidi; Oliveira, Lisandra Brandino de; Menani, José Vanderlei; Callera, João CarlosBackground: Activation of GABAB receptors with baclofen into the lateral parabrachial nucleus (LPBN) induces ingestion of water and 0.3 M NaCl in fluid replete rats. However, up to now, no study has investigated the effects of baclofen injected alone or combined with GABAB receptor antagonist into the LPBN on water and 0.3 M NaCl intake in rats with increased plasma osmolarity (rats treated with an intragastric load of 2 M NaCl). Male Wistar rats with stainless steel cannulas implanted bilaterally into the LPBN were used. Results: In fluid replete rats, baclofen (0.5 nmol/0.2 μl), bilaterally injected into the LPBN, induced ingestion of 0.3 M NaCl (14.3 ± 4.1 vs. saline: 0.2 ± 0.2 ml/210 min) and water (7.1 ± 2.9 vs. saline: 0.6 ± 0.5 ml/210 min). In cell-dehydrated rats, bilateral injections of baclofen (0.5 and 1.0 nmol/0.2 μl) into the LPBN induced an increase of 0.3 M NaCl intake (15.6 ± 5.7 and 21.5 ± 3.5 ml/210 min, respectively, vs. saline: 1.7 ± 0.8 ml/210 min) and an early inhibition of water intake (3.5 ± 1.4 and 6.7 ± 2.1 ml/150 min, respectively, vs. saline: 9.2 ± 1.4 ml/150 min). The pretreatment of the LPBN with 2-hydroxysaclofen (GABAB antagonist, 5 nmol/0.2 μl) potentiated the effect of baclofen on 0.3 M NaCl intake in the first 90 min of test and did not modify the inhibition of water intake induced by baclofen in cell-dehydrated rats. Baclofen injected into the LPBN did not affect blood pressure and heart rate. Conclusions: Thus, injection of baclofen into the LPBN in cell-dehydrated rats induced ingestion of 0.3 M NaCl and inhibition of water intake, suggesting that even in a hyperosmotic situation, the blockade of LPBN inhibitory mechanisms with baclofen is enough to drive rats to drink hypertonic NaCl, an effect independent of changes in blood pressure.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.