Abstract:The aim of the present work was to investigate the role of the serotoninergic system in the control of sodium appetite of hypothyroid rats (HTR) by administering drugs that affect the serotoninergic activity, and to compare the same homeostatic behaviour in euthyroid rats (ETR) also given these drugs. Fenfluramine (FEN; 5.0 mg kg _1 , I.P.), which releases serotonin in the brain, significantly reduced the intake of 1.8 % NaCl in HTR subjected to water and sodium depletion (depleted) or water, sodium and food d… Show more
“…It has been postulated that the DRN serotonergic neurons receive viscerosensory inputs concerning renal sodium load and/or ECF volume variations to trigger homeostatic regulation of sodium appetite (6,21,30). This view has not shown).…”
We determined if the dorsal raphe nucleus (DRN) exerts tonic control of basal and stimulated sodium and water intake. Male Wistar rats weighing 300-350 g were microinjected with phosphate buffer (PB-DRN, N = 11) or 1 µg/0.2 µl, in a single dose, ibotenic acid (IBO-DRN, N = 9 to 10) through a guide cannula into the DRN and were observed for 21 days in order to measure basal sodium appetite and water intake and in the following situations: furosemide-induced sodium depletion (20 mg/kg, sc, 24 h before the experiment) and a low dose of dietary captopril (1 mg/g chow). From the 6th day after ibotenic acid injection IBO-DRN rats showed an increase in sodium appetite (12.0 ± 2.3 to 22.3 ± 4.6 ml 0.3 M NaCl intake) whereas PB-DRN did not exceed 2 ml (P < 0.001). Water intake was comparable in both groups. In addition to a higher dipsogenic response, sodium-depleted IBO-DRN animals displayed an increase of 0.3 M NaCl intake compared to PB-DRN (37.4 ± 3.8 vs 21.6 ± 3.9 ml 300 min after fluid offer, P < 0.001). Captopril added to chow caused an increase of 0.3 M NaCl intake during the first 2 days (IBO-DRN, 33.8 ± 4.3 and 32.5 ± 3.4 ml on day 1 and day 2, respectively, vs 20.2 ± 2.8 ml on day 0, P < 0.001). These data support the view that DRN, probably via ascending serotonergic system, tonically modulates sodium appetite under basal and sodium depletion conditions and/or after an increase in peripheral or brain angiotensin II.
“…It has been postulated that the DRN serotonergic neurons receive viscerosensory inputs concerning renal sodium load and/or ECF volume variations to trigger homeostatic regulation of sodium appetite (6,21,30). This view has not shown).…”
We determined if the dorsal raphe nucleus (DRN) exerts tonic control of basal and stimulated sodium and water intake. Male Wistar rats weighing 300-350 g were microinjected with phosphate buffer (PB-DRN, N = 11) or 1 µg/0.2 µl, in a single dose, ibotenic acid (IBO-DRN, N = 9 to 10) through a guide cannula into the DRN and were observed for 21 days in order to measure basal sodium appetite and water intake and in the following situations: furosemide-induced sodium depletion (20 mg/kg, sc, 24 h before the experiment) and a low dose of dietary captopril (1 mg/g chow). From the 6th day after ibotenic acid injection IBO-DRN rats showed an increase in sodium appetite (12.0 ± 2.3 to 22.3 ± 4.6 ml 0.3 M NaCl intake) whereas PB-DRN did not exceed 2 ml (P < 0.001). Water intake was comparable in both groups. In addition to a higher dipsogenic response, sodium-depleted IBO-DRN animals displayed an increase of 0.3 M NaCl intake compared to PB-DRN (37.4 ± 3.8 vs 21.6 ± 3.9 ml 300 min after fluid offer, P < 0.001). Captopril added to chow caused an increase of 0.3 M NaCl intake during the first 2 days (IBO-DRN, 33.8 ± 4.3 and 32.5 ± 3.4 ml on day 1 and day 2, respectively, vs 20.2 ± 2.8 ml on day 0, P < 0.001). These data support the view that DRN, probably via ascending serotonergic system, tonically modulates sodium appetite under basal and sodium depletion conditions and/or after an increase in peripheral or brain angiotensin II.
“…In this condition, the ACE inhibitor just acts peripherally. Therefore, the increase of brain ANG I availability provides the manifestation of the sodium appetite through mechanism that requires central conversion of ANG I to ANG II (Elfont et al 1984, Moe et al 1984, Fitzsimons 1998, Badauê-Passos et al 2003.…”
Section: Regulationmentioning
confidence: 99%
“…Studies carried out in our laboratory led to similar results. Acute systemic treatments with the brain 5-HT releaser, fenfluramine, the selective 5-HT re-uptake inhibitor, fluoxetine or the 5-HT2C receptor agonists, MK212 and mCPP, reduced signifi cantly the hypertonic saline ingestion, in both, fluids and food deprived-rats and sodium-depleted rats as well (Badauê-Passos et al 2003). Intracerebroventricular administration of 5-HT agonists confi rmed the observations obtained with the systemic treatment and introduced the probable participation of another 5-HT receptor.…”
Section: Lesions Of the Midbrain Raphe Nuclei Brain 5-ht Depletion Amentioning
The present article reviews the role of the serotoninergic system in the regulation of the sodium appetite. Data from the peripheral and icv administration of serotoninergic (5-HTergic) agents showed the participation of 5-HT2/3 receptors in the modulation of sodium appetite. These observations were extended with the studies carried out after brain serotonin depletion, lesions of DRN and during blockade of 5-HT2A/2C receptors in lateral parabrachial nucleus (LPBN). Brain serotonin depletion and lesions of DRN increased the sodium appetite response, in basal conditions, after sodium depletion and hypovolemia or after beta-adrenergic stimulation as well. These observations raised the hypothesis that the suppression of ascending pathways from the DRN, possibly, 5-HTergic fi bers, modifi es the angiotensinergic or sodium sensing mechanisms of the subfornical organ involved in the control of the sodium appetite. 5-HTergic blockade in LPBN induced to similar results, particularly those regarded to the natriorexigenic response evoked by volume depletion or increase of the hypertonic saline ingestion induced by brain angiotensinergic stimulation. In conclusion, many evidences lead to acceptation of an integrated participation resulting of an interaction, between DRN and LPBN, for the sodium appetite control.
“…Behavior, such as drinking and feeding are constantly monitored by 5-HT-containing neurons in mammals and birds. Studies in our laboratory evidenced the serotonergic neurons influence in the sodium appetite and food and water intake behavior (Badauê-Passos Jr et al, 2003;Olivares et al, 2003;Lima et al, 2004;Cavalcante-Lima et al, 2005a,b;Cedraz-Mercez et al, 2005;Medeiros et al, 2005). In rats, peripheral administration of either 5-HT or its precursor 5-HTP induces water intake via renal renin-angiotensin system (RAS) activation (Rowland et al, 1987), however they display opposed effects when centrally applied.…”
Section: General and Experimental Proceduresmentioning
The purpose of this study was to explore the role of L-5-hydroxytryptophan (L-HTP) and its relationship with the reninangiotensin system (RAS) on the drinking behavior in Japanese quails. Normally-hydrated quails that received injections of L-HTP (12.5; 25 and 50 mg.kg -1 ) by the intracoelomic route (ic) expressed an increase in water intake, which was inhibited by captopril, an angiotensin converting enzyme (ACE) inhibitor. In addition, captopril also induced such a response in birds under previous fluid deprivation. High doses of captopril (35-70 mg.kg -1 , sc) in normally-hydrated quails decreased the spontaneous water intake while low doses of captopril (2-5 mg.kg -1 , sc) did not prompt water intake after L-HTP administration. Losartan, an AT 1 receptor antagonist in mammals, did not change the water intake levels in normally-hydrated or water-deprivated birds. Serotonin (5-HT) injections did not provoke its known dipsogenic response.Keywords: drinking behavior, renin-angiotensin system, L-5-hydroxytryptophan, thirst, Coturnix japonica.
Efeito do l-5-hidroxi-triptofano no comportamento dipsogênico em Coturnix japonica(Galliformes: Aves): Envolvimento do sistema renina-angiotensina
ResumoO objetivo deste estudo foi investigar a influência do L-5-hidroxitriptofano (L-HTP) e sua relação com o sistema renina-angiotensina (SRA) no comportamento dipsogênico de codornas. Codornas normohidratadas que receberam L-HTP em diferentes doses (12,5; 25 e 50 mg.kg -1 ) por via intracelomática (ic) expressaram um aumento na ingestão de água, o qual foi suprimido pela administração prévia de captopril (inibidor da ECA-enzima conversora de angiotensina). Esta ação inibitória do captopril, em menor intensidade, foi também evidenciada em aves previamente submetidas ao jejum hídrico. O tratamento isolado com captopril (35-70 mg.kg -1 ) reduziu consideravelmente a ingestão espontânea de água em codornas normohidratadas, enquanto baixas doses (2-5 mg.kg -1 ) não provocaram aumento na ingestão de água induzida pelo L-HTP. Losartan, um antagonista de receptores AT 1 em mamíferos, não foi capaz de modificar os níveis de ingestão hídrica, tanto em aves normohidratadas quanto em aves privadas de água. Serotonina aplicada perifericamente não promoveu a conhecida resposta dipsogênica de mamíferos.Palavras-chave: comportamento dipsogênico, sistema renina-angiotensina, L-5-hidroxitriptofano, sede, Coturnix japonica.
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