Sodium intake by hyperosmotic rats treated with a GABA(A) receptor agonist into the lateral parabrachial nucleus

Inhibitory 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 GABA(A) 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 0.3 M NaCl 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 mu l), 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 mu l) into the LPBN reduced the effect of muscimol on 0.3 M NaCl intake (7.1 +/- 2.1 ml/210 min). Therefore, the activation of GABAA 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. (c) 2007 Elsevier B.V. All rights reserved.

Influence of enamel matrix derivative (Emdogain((R))) and sodium fluoride on the healing process in delayed tooth replantation: histologic and histometric analysis in rats

Although it has already been shown that enamel matrix derivative (Emdogain((R))) promotes periodontal regeneration in the treatment of intrabony periodontal defects, there is little information concerning its regenerative capacity in cases of delayed tooth replantation. To evaluate the alterations in the periodontal healing of replanted teeth after use of Emdogain((R)), the central incisors of 24 Wistar rats (Rattus norvegicus albinus) were extracted and left on the bench for 6 h. Thereafter, the dental papilla and the enamel organ of each tooth were sectioned for pulp removal by a retrograde way and the canal was irrigated with 1% sodium hypochlorite. The teeth were assigned to two groups:in group I, root surface was treated with 1% sodium hypochlorite for 10 min (changing the solution every 5 min), rinsed with saline for 10 min and immersed in 2% acidulated-phosphate sodium fluoride for 10 min; in group II, root surfaces were treated in the same way as described above, except for the application of Emdogain((R)) instead of sodium fluoride. The teeth were filled with calcium hydroxide (in group II right before Emdogain((R)) was applied) and replanted. All animals received antibiotic therapy. The rats were killed by anesthetic overdose 10 and 60 days after replantation. The pieces containing the replanted teeth were removed, fixated, decalcified and paraffin-embedded. Semi-serial 6-mu m-thick sections were obtained and stained with hematoxylin and eosin for histologic and histometric analyses. The use of 2% acidulated-phosphate sodium fluoride provided more areas of replacement resorption. The use of Emdogain((R)) resulted in more areas of ankylosis and was therefore not able to avoid dentoalveolar ankylosis. It may be concluded that neither 2% acidulated-phosphate sodium fluoride nor Emdogain((R)) were able to prevent root resorption in delayed tooth replantation in rats.

Effect of Sodium Ascorbate on Tag Formation in Bleached Enamel

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Anticaries effect of dentifrices with calcium citrate and sodium trimetaphosphate

Because of the growing concerns regarding fluoride ingestion by young children and dental fluorosis, it is necessary to develop new dentifrices. Objective: The aim of this study was to evaluate the effect of dentifrices with calcium citrate (Cacit) and sodium trimetaphosphate (TMP) on enamel demineralization. Material and Methods: Enamel blocks (n=70), previously selected through surface hardness analysis, were submitted to daily treatment with dentifrices diluted in artificial saliva and to a pH-cycling model. The fluoride concentration in dentifrices was 0, 250, 450, 550, 1,000 and 1,100 mu g F/g. Crest (TM) was used as a positive control (1,100 mu g F/g). Cacit (0.25%) and TMP (0.25%) were added to dentifrices with 450 and 1,000 mu g F/g. Surface hardness was measured again and integrated loss of subsurface hardness and fluoride concentration in enamel were calculated. Parametric and correlation tests were used to determine difference (p<0.05) and dose-response relationship between treatments. Results: The addition of Cacit and TMP did not provide a higher fluoride concentration in enamel, however it reduced (p<0.05) mineral loss when compared to other dentifrices; the dentifrice with Cacit and TMP and a low fluoride concentration presented similar results when compared to a dentifrice with 1,100 mu g F/g (p>0.05). Conclusions: Dentifrices with 450 and 1,000 mu g F/g, Cacit and TMP were as effective as a gold standard one.

Transdentinal protective role of sodium ascorbate against the cytopathic effects of H2O2 released from bleaching agents

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

Interaction between supraoptic nucleus and septal area in the control of water, sodium intake and arterial blood pressure induced by injection of angiotensin II

We investigated the effects of injection into the supraoptic nucleus (SON) of losartanand PD 123319 (nonpeptide AT(1) and AT(2)- angiotensin II [ANG II] receptor antagonists, respectively); d(CH2)(5)-Tyr(Me)-AVP (AVPA; an arginine-vasopressin [AVP] V-1 receptor antagonist), FK 409 (a nitric oxide [NO] donor), and N-W-mtro-(L)-arginine methyl ester ((L)-NAME; an NO synthase inhibitor) oil water intake, sodium chloride 3% (NaCl) intake and arterial blood pressure induced by injection of ANG 11 into the lateral septal area (LSA). Mate Holtzman rats (250-300 g) were implanted with cannulae into SON and LSA unilaterally. The drugs were injected in 0.5 mul over 30-60 s. Controls were injected with a similar volume of 0.15 M NaCl. ANG II was injected at a dose of 10 pmol. ANG II antagonists and AVPA were injected at doses of 80 nmol. FK 409 and (L)-NAME were injected at doses of 20 and 40 mug, respectively. Water and NaCl intake was measured over a 2-h period. Prior administration of losartan into the SON decreased water and NaCl intake induced by injection of ANG II. While there was a decrease in water intake, ANG II-induced NaCl intake was significantly increased following injection of AVPA. FK 409 injection decreased water intake and sodium intake induced by ANG II. L-NAME alone increased water and sodium intake and induced a pressor effect. (L)-NAME-potentiated water and sodium intake induced by ANG II. PD 123319 produced no changes in water or sodium intake induced by ANG II. The prior administration of losartan or AVPA decreased mean arterial pressure (MAP) induced by ANG II. PD 123319 decreased the pressor effect of ANG II to a lesser degree than losartan. FK 409 decreased the pressor effect of ANG II while (L)-NAME potentiated it. These results suggest that both ANG II AT, and AVP V, receptors and NO within the SON may be involved in water intake, NaCl intake and the pressor response were induced by activation of ANG II receptors within the LSA. These results do not support the involvement of LSA AT(2) receptors in the mediation of water and NaCl intake responses induced by ANG II, but influence the pressor response. (C) 2004 Elsevier B.V. All rights reserved.

Interaction between arginine vasopressin and angiotensin II receptors in the central regulation of sodium balance

We speculated that the influence of lateral preoptic area (LPO) in sodium balance, involves arginine(8)-vasopressin (AVP) and angiotensin (ANG II) on Na+ uptake in LPO. Therefore, the present study investigated the effects of central administration of specific AVP and ANG 11 antagonists (d(CH2)(5)-Tyr (Me)-AVP (AAVP) and [Adamanteanacetyl(1), 0-ET-D-Tyr(2), Val(4), Aminobutyryl(6), Arg(8.9)]-AVP (ATAVP) antagonists of V-1 and V-2 receptors of AVP. Also the effects of losartan and CGP42112A (selective ligands of the AT(1) and AT(2) angiotensin receptors, respectively), was investigated on Na+ uptake and renal fluid and electrolyte excretion. After an acclimatization period of 7 days, the animals were maintained under tribromoethanol (200 mg/kg body weight, intraperitonial) anesthesia and placed in a Kopf stereotaxic instrument. Stainless guide cannula was implanted into the LPO. AAVP and ATAVP injected into the LPO prior to AVP produced a reduction in the NaCl intake. Both the AT(1) and AT(2) ligands administered into the LPO elicited a decrease in the NaCl intake induced by AVP injected into the LPO. AVP injection into the LPO increased sodium renal excretion, but this was reduced by prior AAVP administration. The ATAVP produced a decreased in the natriuretic effect of AVP. The losartan injected into LPO previous to AVP decreased the sodium excretion and the CGP 421122A also decreased the natriuretic effect of AVP. The AVP produced an antidiuresis effect that was inhibited by prior administration into LPO of the ATAVP. The AAVP produced no change in the antidiuretic effect of AVP. These results suggest that LPO are implicated in sodium balance that is mediated by V-1, V-2, AT(2) and AT(2) receptors. (c) 2005 Elsevier B.V All rights reserved.

Vasopressin and angiotensin receptors of the medial septal area of the brain in the control of thirst and salt appetite induced by vasopressin in water-deprived and sodium-depleted rats

In this study we investigated the influence of d(CH2)(5)-Tyr (Me)-AVP (A(1) AVP) and [Adamanteanacatyl(1),D-ET-D-Tyr(2), Va1(4), aminobutyril(6) ,As-8,As-9]-AVP 9 (A(2)AVP), antagonists of V-1 and V-2 arginine(8)-vasopressin (AVP) receptors, respectively, as well as the effects of losartan and CGP42112A, antagonists of angiotensin II (ANGII) AT(1) and AT(2), receptors, respectively, on water and 0.3 M sodium intake induced by water deprivation or sodium depletion (furosemide treatment) and enhanced by AVP injected into the medial septal area (N4SA). A stainless steel carmulawas implanted into the medial septal area (NISA) of male Holtzman rats AVP injection enhanced water and sodium intake in a dose-dependent manner. Pretreatment with V-1 antagonist injected into the MSA produced a dose-dependent reduction, whereas prior injection of V-2 antagonist increased, in a dose-dependent manner, the water and sodium responses elicited by the administration of AVP. Both AT(1) and AT(2) antagonists administered into the MSA elicited a concentration-dependent decrease in water and sodium intake induced by AVP, while simultaneous injection of the two antagonists was more effective in decreasing AVP responses. These results also indicate that the increase in water and sodium intake induced by AvT was mediated primarily by MSA AT(1) receptors. (c) 2007 Published by Elsevier B.V.

Noradrenaline and mixed alpha(2)-adrenoceptor/imidazoline-receptor ligands: effects on sodium intake

The effect of noradrenaline, and mixed ligands to alpha(2)-adrenoceptors (alpha(2)-AR) and imidazoline receptors (IR), injected intracerebroventricularly (i.c.v.), on sodium intake of sodium depleted rats, was tested against idazoxan, a mixed antagonist ligand to alpha(2)-AR and IR. The inhibition of sodium intake induced by noradrenaline (80 nmol) was completely reversed by idazoxan (160 and 320 nmol) injected i.c.v. The inhibition of sodium intake induced by mixed ligands to alpha(2)-AR and IR, UK14,304, guanabenz and moxonidine, was antagonized from 50 to 60% by idazoxan i.c.v. The results demonstrate that noradrenaline, a non-ligand for IR, acts on alpha(2)-AR inhibiting sodium intake. The possibility that either alpha(2)-AR or IR mediate the effect of mixed agonists on sodium intake remains an open question. (C) 1999 Elsevier B.V. B.V. All rights reserved.

Interaction of serotonin and cholecystokinin in the lateral parabrachial nucleus to control sodium intake

Serotonin [5-hydroxytryptamine (5-HT)] and CCK injected into the lateral parabrachial nucleus (LPBN) inhibit NaCl and water intake. In this study, we investigated interactions between 5-HT and CCK into the LPBN to control water and NaCl intake. Male Holtzman rats with cannulas implanted bilaterally in the LPBN were treated with furosemide + captopril to induce water and NaCl intake. Bilateral LPBN injections of high doses of the 5-HT antagonist methysergide (4 mug) or the CCK antagonist proglumide (50 mug), alone or combined, produced similar increases in water and 1.8% NaCl intake. Low doses of methysergide (0.5 mug) + proglumide (20 mug) produced greater increases in NaCl intake than when they were injected alone. The 5-HT2a/2c agonist 2,5-dimetoxy-4-iodoamphetamine hydrobromide (DOI; 5 mug) into the LPBN reduced water and NaCl intake. After proglumide (50 mug) + DOI treatment, the intake was not different from vehicle treatment. CCK-8 (1 mug) alone produced no effect. CCK-8 combined with methysergide (4 mug) reduced the effect of methysergide on NaCl intake. The data suggest that functional interactions between 5-HT and CCK in the LPBN may be important for exerting inhibitory control of NaCl intake.

5-HT2 and 5-HT3 receptors in the lateral parabrachial nucleus mediate opposite effects on sodium intake

The present study investigated the role of several 5-HT receptor subtypes in the lateral parabrachial nucleus (LPBN) in the control of sodium appetite (i.e. NaCl consumption). Male Holtzman rats had cannulas implanted bilaterally into the LPBN for the injection of 5-HT receptor agonists and antagonists in conjunction with either acute fluid depletion or 24-h sodium depletion. Following these treatments, access to 0.3 M NaCl was provided and the intakes of saline and water were measured for the next 2 h. Bilateral injections of the 5-HT2A receptor antagonist, ketanserin or the 5-HT2C receptor antagonist, mianserin into the LPBN increased 0.3 M NaCl intake without affecting water intake induced by acute fluid-depletion. Bilateral injections of the 5-HT2B receptor agonist, BW723C86 hydrochloride, had no effect on 0.3 M NaCl or water intake under these conditions. Treatment of the LPBN with the 5-HT2B/2C receptor agonist, 2-(2-methyl-4-clorophenoxy) propanoic acid (mCPP) caused dose-related reductions in 0.3 M NaCl intake after 24 h sodium depletion. The effects of mCPP were prevented by pretreating the LPBN with the 5-HT2B/2C receptor antagonist, SDZSER082. Activation of 5-HT3 receptors by the receptor agonist, 1-phenylbiguanicle (PBG) caused dose-related increases in 0.3 M NaCl intake. Pretreatment of the LPBN with the 5-HT3 receptor antagonist, 1-methyl-N-[8-methyl-8-azabicyclo (3.2.1)-oct-3-yl]-1H-indazole-3-carboxamide (LY-278,584) abolished the effects of PBG, but LY-278,584 had no effects on sodium or water intake when injected by itself. PBG injected into the LPBN did not alter intake of palatable 0.06 M sucrose in fluid replete rats. The results suggest that activation of the 5-HT2A and 5-HT2C receptor subtypes inhibits sodium ingestion. In contrast, activation of the 5-HT3 receptor subtype increases sodium ingestion. Therefore, multiple serotonergic receptor subtypes in the LPBN are implicated in the control of sodium intake, sometimes by mediating opposite effects of 5-HT. The results provide new information concerning the control of sodium intake by LPBN mechanisms. (C) 2007 IBRO. Published by Elsevier Ltd. All rights reserved.

Serotonergic mechanisms of the lateral parabrachial nucleus on DOCA-induced sodium intake

It has been shown that the serotonergic mechanisms of the lateral parabrachial nucleus (LPBN) inhibit NaCl intake in different models of angiotensin II (ANG II)-dependent NaCl intake in rats. However, there is no information about the involvement of LPBN serotonergic mechanisms on NaCl intake in a model of NaCl intake not dependent on ANG II like deoxycorticosterone (DOCA)-induced NaCl intake. Therefore, in this study we investigated the effects of bilateral injections of serotonergic agonist and antagonist into the LPBN on DOCA-induced 1.8% NaCl intake in rats. Male Holtzman rats were treated with s.c. DOCA (10 mg/rat each every 3 days). After a period of training, in which the rats had access to 1.8% NaCI during 2 h for several days, the rats were implanted with stainless steel cannulas bilaterally into the LPBN. Bilateral injections of the serotonergic receptor antagonist methysergide (4 mug/0.2 mul each site) in the LPBN increased 1.8% NaCI intake (32.2+/-3.9 versus vehicle: 15.0+/-1.6 ml/2 h, n = 10) and water intake (11.5+/-3.5 versus vehicle: 3.2+/-1.0 ml/2 h). Injections of the serotonergic 5HT(2A/2C) receptor agonist DOI (5 mug/0,2 mul each site) in the LPBN reduced 1.8% NaCl intake (6.8+/-1.7 versus saline: 12.4+/-1.9 ml/2 h, n = 10) and water intake (2.2+/-0.8 versus saline: 4.4+/-1.0 ml/2 h). Besides the previously demonstrated importance for the control of ANG II-dependent water and NaCl intake, the data show that the serotonergic inhibitory mechanisms of the LPBN are also involved in the control of DOCA-induced NaCl intake. (C) 2000 Elsevier B.V. B.V. All rights reserved.