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Laura Vivas - One of the best experts on this subject based on the ideXlab platform.
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acute body Sodium Depletion induces skin Sodium mobilization in female wistar rats
Experimental Physiology, 2019Co-Authors: V C Lopesmenezes, Laura Vivas, Raoni C Dossantos, V Felintro, Livia Monteiro, Bruno Paesleme, Danilo Lustrino, E A Casartelli, Andre S MecawiAbstract:NEW FINDINGS What is the central question of this study? Can Na+ Depletion mobilize Na+ from the skin reservoir in ovariectomized rats? Does oestrogen replacement change the amount and the dynamics of skin Na+ storage? Is the reduced salt appetite after Na+ Depletion in ovariectomized rats with oestrogen replacement related to changes in the skin Na+ ? What is the main finding and its importance? This work demonstrated that acute body Na+ Depletion induced by frusemide mobilized the osmotically inactive skin Na+ reservoir to become osmotically active. Oestrogen treatment decreased the induced Na+ intake in ovariectomized rats but did not modulate the inactive Na+ reservoir in control conditions or its mobilization induced by Na+ Depletion. ABSTRACT Oestradiol, which is an important hormone for water and electrolyte balance, also has a role in the inhibition of induced Na+ appetite. Sodium can be stored in the skin in osmotically active or inactive forms, and this skin Na+ reservoir may be involved in the control of body Na+ levels during physiopathological challenges. In this study, we investigated whether the effect of Sodium Depletion by frusemide can mobilize Na+ from the skin reservoir and whether oestradiol replacement changes or mobilizes the Na+ reserves in the skin. Ovariectomized Wistar rats were treated with vehicle or oestradiol for 7 days to evaluate the effects of oestrogen on the hydroelectrolyte balance, intake responses and skin Na+ and water content in basal conditions. Furthermore, the effects of oestrogen were evaluated after 24 h frusemide-induced whole-body Na+ Depletion. Oestradiol-replaced rats exhibited reduced water intake without any significant changes in salt intake, Na+ excretion or water and Na+ skin content in basal conditions. After Sodium Depletion, both vehicle- and oestradiol-treated rats exhibited an increase in the osmotically active skin Na+ , which was associated with a decrease of the inactive skin Na+ reservoir. Oestrogen decreased the hypertonic saline intake induced by Na+ Depletion, but it was not associated with any significant changes in the skin Na+ reservoir. Thus, Sodium Depletion is able to change the inactive-active skin Na+ reservoir balance. However, the oestrogenic modulation of Sodium appetite after Na+ Depletion is probably not related to the action of this hormone in the skin Na+ reservoir balance.
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whole body Sodium Depletion modifies at1 mrna expression and serotonin content in the dorsal raphe nucleus
Journal of Neuroendocrinology, 2019Co-Authors: Cintia Yamila Porcari, Jose Vanderlei Menani, Iracema G Araujo, Lilia Urzedorodrigues, Laurival A De Luca, Ximena E Caeiro, Hans Imboden, Jose Antunesrodrigues, L C Reis, Laura VivasAbstract:Angiotensin II (Ang II) acts on Ang II type 1 (AT1) receptors located in the organum vasculosum and subfornical organ (SFO) of the lamina terminalis as a main facilitatory mechanism of Sodium appetite. The brain serotonin (5-HT) system with soma located in the dorsal raphe nucleus (DRN) provides a main inhibitory mechanism. In the present study, we first investigated the existence of Ang II AT1 receptors in serotonergic DRN neurones. Then, we examined whether whole body Sodium Depletion affects the gene expression of the AT1a receptor subtype and the presumed functional significance of AT1 receptors. Using confocal microscopy, we found that tryptophan hydroxylase-2 and serotonin neurones express AT1 receptors in the DRN. Immunofluorescence quantification showed a significant reduction in 5-HT content but no change in AT1 receptor expression or AT1/5-HT colocalisation in the DRN after Sodium Depletion. Whole body Sodium Depletion also significantly increased Agtr1a mRNA expression in the SFO and DRN. Oral treatment with the AT1 receptor antagonist losartan reversed the changes in Agtr1a expression in the SFO but not the DRN. Losartan injection into either the DRN or the mesencephalic aqueduct had no influence on Sodium Depletion-induced 0.3 mol L-1 NaCl intake. The results indicate the expression of Agtr1a mRNA in the DRN and SFO as a marker of Sodium Depletion. They also suggest that serotonergic DRN neurones are targets for Ang II. However, the function of their AT1 receptors remains elusive.
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sex differences in body fluid homeostasis sex chromosome complement influences on bradycardic baroreflex response and Sodium Depletion induced neural activity
Physiology & Behavior, 2015Co-Authors: Laura Vivas, Florencia M Dadam, Ximena E CaeiroAbstract:Clinical and basic findings indicate that angiotensin II (ANG II) differentially modulates hydroelectrolyte and cardiovascular responses in male and female. But are only the activational and organizational hormonal effects to blame for such differences? Males and females not only differ in their sex (males are born with testes and females with ovaries) but also carry different sex chromosome complements and are thus influenced throughout life by different genomes. In this review, we discuss our recent studies in order to evaluate whether sex chromosome complement is in part responsible for gender differences previously observed in ANG II bradycardic-baroreflex response and Sodium Depletion-induced Sodium appetite and neural activity. To test the hypothesis that XX or XY contributes to the dimorphic ANG II bradycardic-baroreflex response, we used the four core genotype mouse model, in which the effects of gonadal sex (testes or ovaries) and sex chromosome complement (XX or XY) are dissociated. The results indicate that ANG II bradycardic-baroreflex sexual dimorphic response may be ascribed to differences in sex chromosomes, indicating an XX-sex chromosome complement facilitatory bradycardic-baroreflex control of heart rate. Furthermore, we evaluated whether genetic differences within the sex chromosome complement may differentially modulate the known sexually dimorphic Sodium appetite as well as basal or induced brain activity due to physiological stimulation of the renin-angiotensin system by furosemide and low-Sodium treatment. Our studies demonstrate an organizational hormonal effect on sexually dimorphic induced Sodium intake in mice, while at the brain level (subfornical organ and area postrema) we showed a sex chromosome complement effect in Sodium-depleted mice, suggesting a sex chromosome gene participation in the modulation of neural pathways underlying regulatory response to renin-angiotensin stimulation.
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temporal dissociation between Sodium Depletion and Sodium appetite appearance involvement of inhibitory and stimulatory signals
Neuroscience, 2015Co-Authors: Lisandra Oliveira Margatho, Ximena E Caeiro, Jose Antunesrodrigues, Laura Vivas, C Y Porcari, Ana Fabiola Macchione, G D Da Silva Souza, Andrea GodinoAbstract:Abstract Our aim was to analyze the participation of inhibitory and stimulatory signals in the temporal dissociation between Sodium Depletion (SD) induced by peritoneal dialysis (PD) and the appearance of Sodium appetite (SA), particularly 2 h after PD, when the rats are hypovolemic/natremic but SA is not evident. We investigated the effects of bilateral injections of the serotonin (5-HT) receptor antagonist, methysergide, into the lateral parabrachial nucleus (LPBN) on hypertonic NaCl and water intake 2 h vs. 24 h after PD. We also studied plasma renin activity (PRA) and aldosterone (ALDO) concentration 2 h vs. 24 h after PD. Additionally, we combined the analysis of brain Fos immunoreactivity (Fos-ir) with the detection of double immunoreactivity in 5HT and oxytocinergic (OT) cells 2 h after PD. Bilateral LPBN injections of methysergide (4 μg/200 nl at each site) increased NaCl intake when tested 2 h after PD compared to controls. We found a significant increase in PRA and ALDO concentration after PD but no differences between 2 and 24 h after PD. We also found for the first time a significant increase 2 h after PD in the number of Fos-ir neurons in the brainstem nuclei that have been shown to be involved in the inhibition of SA. In summary, the results show that 5HT-mechanisms in the LPBN modulate Sodium intake during the delay of SA when the renin angiotensin aldosterone system (RAAS) is increased. In addition, the activation of brainstem areas previously associated with the satiety phase of SA is in part responsible for the temporal dissociation between SD and behavioral arousal.
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Sodium Depletion induces fos immunoreactivity in circumventricular organs of the lamina terminalis
Brain Research, 1995Co-Authors: Laura Vivas, Cinthia Veronica Pastuskovas, Leonardo TonelliAbstract:Abstract Acute Sodium Depletion by peritoneal dialysis (PD) induces c- fos expression in the subfornical organ (SFO) and organum vasculosum laminae terminalis (OVLT), in conscious rats. Fos immunoreactive (Fos-ir) neurons detected by immunohistochemistry first appeared in these nuclei 60 min after PD, increased gradually in the next 4 h and remained high for 27 h following PD. Fos-ir cells were distributed throughout the body of SFO, being the core of the posterior sections preferentially activated, whereas Fos-ir neurons occurred around the periphery of OVLT (annular disposition). When rats were allowed to drink Sodium salt (1.8% NaCl) 24 h after PD, there was a marked reversion of the c- fos expression in the OVLT and a comparatively smaller effect in the SFO. Intracerebroventricular infusion of hypertonic CSF (170 mM NaCl) from 30 min before and during 4 h after PD, significantly inhibited the c- fos expression in both nuclei. These results demonstrate that an acute body Sodium deficit induces c- fos activity in SFO and OVLT neurons, indicating the special role of these structures in Sodium balance regulation. They also show that the Sodium-Depletion-induced production of Fos in neurons of the lamina terminalis can be modulated by central or systemic reposition of Sodium.
M J Mckinley - One of the best experts on this subject based on the ideXlab platform.
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adaptive appetites for salted and unsalted food in rats differential effects of Sodium Depletion doca and dehydration
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2013Co-Authors: M J MckinleyAbstract:Most ingested Sodium is contained in food. The aim was to investigate whether Sodium Depletion, dehydration, or DOCA alters intakes of salted and unsalted foods by rats given choices of two foods: ...
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adaptive appetites for salted and unsalted food in rats differential effects of Sodium Depletion doca and dehydration
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2013Co-Authors: M J MckinleyAbstract:Most ingested Sodium is contained in food. The aim was to investigate whether Sodium Depletion, dehydration, or DOCA alters intakes of salted and unsalted foods by rats given choices of two foods: salted (0.2–0.5% Na) and unsalted food containing either similar or different other dietary components. Diuretic-induced (furosemide or acetazolamide, two treatments on successive days) Sodium Depletion always caused pronounced falls in intake of unsalted food within 24 h, continuing at least another 2 days (e.g., 20.9 ± 1.6 pretreatment to 14.8 ± 1.2, 10.6 ± 1.5, and 14.3 ± 1.3 g/day for 3 days of Depletion). Intake and preference for salted food increased after 24–72 h (e.g., 6.5 ± 1.2 pretreatment to 7.1 ± 1.1, 16.4 ± 2.3, and 17.0 ± 1.5 g/day at 1, 2, and 3 days of Depletion). Valsartan (10 mg/day) blocked the increased intake of salted food but not the reduced intake of unsalted food. DOCA (2 mg/day) caused equivalent increase and decrease in intakes of salted and unsalted food, respectively. Water-deprived...
Ximena E Caeiro - One of the best experts on this subject based on the ideXlab platform.
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whole body Sodium Depletion modifies at1 mrna expression and serotonin content in the dorsal raphe nucleus
Journal of Neuroendocrinology, 2019Co-Authors: Cintia Yamila Porcari, Jose Vanderlei Menani, Iracema G Araujo, Lilia Urzedorodrigues, Laurival A De Luca, Ximena E Caeiro, Hans Imboden, Jose Antunesrodrigues, L C Reis, Laura VivasAbstract:Angiotensin II (Ang II) acts on Ang II type 1 (AT1) receptors located in the organum vasculosum and subfornical organ (SFO) of the lamina terminalis as a main facilitatory mechanism of Sodium appetite. The brain serotonin (5-HT) system with soma located in the dorsal raphe nucleus (DRN) provides a main inhibitory mechanism. In the present study, we first investigated the existence of Ang II AT1 receptors in serotonergic DRN neurones. Then, we examined whether whole body Sodium Depletion affects the gene expression of the AT1a receptor subtype and the presumed functional significance of AT1 receptors. Using confocal microscopy, we found that tryptophan hydroxylase-2 and serotonin neurones express AT1 receptors in the DRN. Immunofluorescence quantification showed a significant reduction in 5-HT content but no change in AT1 receptor expression or AT1/5-HT colocalisation in the DRN after Sodium Depletion. Whole body Sodium Depletion also significantly increased Agtr1a mRNA expression in the SFO and DRN. Oral treatment with the AT1 receptor antagonist losartan reversed the changes in Agtr1a expression in the SFO but not the DRN. Losartan injection into either the DRN or the mesencephalic aqueduct had no influence on Sodium Depletion-induced 0.3 mol L-1 NaCl intake. The results indicate the expression of Agtr1a mRNA in the DRN and SFO as a marker of Sodium Depletion. They also suggest that serotonergic DRN neurones are targets for Ang II. However, the function of their AT1 receptors remains elusive.
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sex differences in body fluid homeostasis sex chromosome complement influences on bradycardic baroreflex response and Sodium Depletion induced neural activity
Physiology & Behavior, 2015Co-Authors: Laura Vivas, Florencia M Dadam, Ximena E CaeiroAbstract:Clinical and basic findings indicate that angiotensin II (ANG II) differentially modulates hydroelectrolyte and cardiovascular responses in male and female. But are only the activational and organizational hormonal effects to blame for such differences? Males and females not only differ in their sex (males are born with testes and females with ovaries) but also carry different sex chromosome complements and are thus influenced throughout life by different genomes. In this review, we discuss our recent studies in order to evaluate whether sex chromosome complement is in part responsible for gender differences previously observed in ANG II bradycardic-baroreflex response and Sodium Depletion-induced Sodium appetite and neural activity. To test the hypothesis that XX or XY contributes to the dimorphic ANG II bradycardic-baroreflex response, we used the four core genotype mouse model, in which the effects of gonadal sex (testes or ovaries) and sex chromosome complement (XX or XY) are dissociated. The results indicate that ANG II bradycardic-baroreflex sexual dimorphic response may be ascribed to differences in sex chromosomes, indicating an XX-sex chromosome complement facilitatory bradycardic-baroreflex control of heart rate. Furthermore, we evaluated whether genetic differences within the sex chromosome complement may differentially modulate the known sexually dimorphic Sodium appetite as well as basal or induced brain activity due to physiological stimulation of the renin-angiotensin system by furosemide and low-Sodium treatment. Our studies demonstrate an organizational hormonal effect on sexually dimorphic induced Sodium intake in mice, while at the brain level (subfornical organ and area postrema) we showed a sex chromosome complement effect in Sodium-depleted mice, suggesting a sex chromosome gene participation in the modulation of neural pathways underlying regulatory response to renin-angiotensin stimulation.
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temporal dissociation between Sodium Depletion and Sodium appetite appearance involvement of inhibitory and stimulatory signals
Neuroscience, 2015Co-Authors: Lisandra Oliveira Margatho, Ximena E Caeiro, Jose Antunesrodrigues, Laura Vivas, C Y Porcari, Ana Fabiola Macchione, G D Da Silva Souza, Andrea GodinoAbstract:Abstract Our aim was to analyze the participation of inhibitory and stimulatory signals in the temporal dissociation between Sodium Depletion (SD) induced by peritoneal dialysis (PD) and the appearance of Sodium appetite (SA), particularly 2 h after PD, when the rats are hypovolemic/natremic but SA is not evident. We investigated the effects of bilateral injections of the serotonin (5-HT) receptor antagonist, methysergide, into the lateral parabrachial nucleus (LPBN) on hypertonic NaCl and water intake 2 h vs. 24 h after PD. We also studied plasma renin activity (PRA) and aldosterone (ALDO) concentration 2 h vs. 24 h after PD. Additionally, we combined the analysis of brain Fos immunoreactivity (Fos-ir) with the detection of double immunoreactivity in 5HT and oxytocinergic (OT) cells 2 h after PD. Bilateral LPBN injections of methysergide (4 μg/200 nl at each site) increased NaCl intake when tested 2 h after PD compared to controls. We found a significant increase in PRA and ALDO concentration after PD but no differences between 2 and 24 h after PD. We also found for the first time a significant increase 2 h after PD in the number of Fos-ir neurons in the brainstem nuclei that have been shown to be involved in the inhibition of SA. In summary, the results show that 5HT-mechanisms in the LPBN modulate Sodium intake during the delay of SA when the renin angiotensin aldosterone system (RAAS) is increased. In addition, the activation of brainstem areas previously associated with the satiety phase of SA is in part responsible for the temporal dissociation between SD and behavioral arousal.
Douglas A Fitts - One of the best experts on this subject based on the ideXlab platform.
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effects of forebrain circumventricular organ ablation on drinking or salt appetite after Sodium Depletion or hypernatremia
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 2004Co-Authors: Douglas A Fitts, Julia A Freece, Julie E Van Bebber, Dannielle Zierath, John E BassettAbstract:In many previous studies, one or the other forebrain circumventricular organ, the subfornical organ (SFO) or organum vasculosum laminae terminalis (OVLT), was lesioned to test whether it was critical for the behavioral or physiological responses to Sodium Depletion and hypernatremia. These studies conflict in their conclusions. The present study was designed to create discrete lesions of both the SFO and OVLT in the same animals and to compare these with rats having a lesion of only the SFO or OVLT. Both the OVLT-lesioned group and the combined SFO + OVLT-lesioned group drank significantly more water and saline on a daily basis than Controls or SFO-lesioned rats. In both Sodium Depletion and hypertonic saline testing, rats with SFO lesions displayed transient deficits in salt appetite or thirst responses, whereas the rats with single OVLT lesions did not. In the Sodium Depletion test, but not in the hypernatremia test, rats with lesions of both the SFO and OVLT exhibited the largest deficit. The data support the hypothesis that a combined lesion eliminates redundancy and is more effective than a single lesion in Sodium Depletion tests. The interpretation of the OVLT lesion-only data may have been complicated by a tendency to drink more fluid on a daily basis, because some of those animals drank copious water in addition to saline even very early during the salt appetite test.
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drinking and blood pressure during Sodium Depletion or ang ii infusion in chronic cholestatic rats
American Journal of Physiology-regulatory Integrative and Comparative Physiology, 1999Co-Authors: Douglas A Fitts, Jeannine R Lane, Elizabeth M StarbuckAbstract:After a chronic ligation of the common bile duct (BDL), Long-Evans rats are hypotensive and have elevated saline intake during both Sodium-depleted and nondepleted conditions. We tested whether BDL rats have exaggerated hypotension during Sodium Depletion or an elevated dipsogenic response to angiotensin II (ANG II) that might help to explain the saline intake. After 4 wk of BDL, rats were hypotensive at baseline and developed exaggerated hypotension during acute furosemide-induced diuresis. Without saline to drink, BDL rats increased water intake during Depletion equal to sham-ligated rats. However, with saline solution available at 22 h after Sodium Depletion, the BDL rats drank more water and saline than did sham-ligated rats. This rapid intake temporarily increased their mean arterial pressure to equal that of sham-ligated rats. Intravenous infusion of ANG II induced equal drinking responses despite reduced pressor responses in the BDL rats relative to sham-ligated rats during both ad libitum and Sodium-depleted conditions. Thus BDL rats have exaggerated hypotension during diuresis, and their hypotension is corrected by drinking an exaggerated volume of saline, but they do not have an increased drinking response to ANG II.
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Influence of Salt Intake, ANG II Synthesis and SFO Lesion on Thirst and Blood Pressure During Sodium Depletion ☆
Appetite, 1998Co-Authors: E.m Starbuck, Douglas A FittsAbstract:Water intake was elevated in Sodium-depleted rats during a daytime salt appetite test, but other rats drank a similar amount of water when saline was not available for drinking during the test. This water intake stimulated by Sodium Depletion was blocked by an inhibition of angiotensin (ANG) II synthesis with a high dose of captopril (100 mg/kg, sc). Captopril did not reduce water intake by causing hypotensive shock or uremia, because water and saline intakes were increased rather than decreased after a low dose of captopril (5 mg/kg) that also reduced blood pressure and elevated blood urea nitrogen. The water intake, but not salt appetite, induced by Sodium Depletion was greatly reduced by a lesion of the subfornical organ (SFO) in one-bottle tests, and this was not clearly related to any effects of the lesion on blood pressure. A physiological role for ANG II in water intake induced by Sodium Depletion has recently been disputed, but the simplest explanation for the data remains that elevated levels of circulating ANG II bind to receptors in the SFO to generate daytime water drinking during Sodium Depletion.
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interaction of hydration and subfornical organ lesions in Sodium Depletion induced salt appetite
Behavioral Neuroscience, 1997Co-Authors: Elizabeth M Starbuck, Jeannine R Lane, Douglas A FittsAbstract:The authors tested whether the level of hydration after furosemide diuresis and 22 hr of Sodium Depletion affects the amount of water or 0.3 M NaCl solution consumed by rats with intact brains or with lesions of the subfornical organ (SFO). Rats received 2 (underhydrated) or 10 (euhydrated) ml/kg water by gavage as the only fluid input 2, 4, and 20 hr after 10 mg/kg furosemide. These hydration treatments had little or no effect on the amount of saline consumed in 2 hr by intact rats. SFO lesions reduced water intake regardless of hydration condition. Euhydrated, SFO-lesioned rats drank a normal amount of saline, but underhydrated, lesioned rats drank less saline than any other group. Thus, euhydration may facilitate salt appetite in SFO-lesioned rats, and the deficits in salt appetite noted in SFO-lesioned rats may result from deficits in water ingestion rather than from a destruction of angiotensin II receptor sites that directly provoke salt appetite.
Xuejuan Yang - One of the best experts on this subject based on the ideXlab platform.
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Involvement of brain ANG II in acute Sodium Depletion induced salty taste changes.
Regulatory peptides, 2012Co-Authors: Jianqun Yan, Xuejuan Yang, Ke ChenAbstract:Many investigations have been devoted to determining the role of angiotensin II (ANG II) and aldosterone (ALD) in Sodium-Depletion-induced Sodium appetite, but few were focused on the mechanisms mediating the salty taste changes accompanied with Sodium Depletion. To further elucidate the mechanism of renin-angiotensin-aldosterone system (RAAS) action in mediating Sodium intake behavior and accompanied salty taste changes, the present study examined the salty taste function changes accompanied with Sodium Depletion induced by furosemide (Furo) combined with different doses of angiotensin converting enzyme (ACE) inhibitor, captopril (Cap). Both the peripheral and central RAAS activity and the nuclei Fos immunoreactivity (Fos-ir) expression in the forebrain area were investigated. Results showed that Sodium Depletion induced by Furo+low-Cap increased taste preference for hypertonic NaCl solution with amplified brain action of ANG II but without peripheral action, while Furosemide combined with a high dose of captopril can partially inhibit the formation of brain ANG II, with parallel decreased effects on salty taste changes. And the resulting elevating forebrain ANG II may activate a variety of brain areas including SFO, PVN, SON and OVLT in Sodium depleted rats injected with Furo+low-Cap, which underlines salty taste function and Sodium intake behavioral changes. Neurons in SFO and OVLT may be activated mainly by brain ANG II, while PVN and SON activation may not be completely ANG II dependent. These findings suggested that forebrain derived ANG II may play a critical role in the salty taste function changes accompanied with acute Sodium Depletion.
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Effects of Sodium Depletion on detection thresholds for salty taste in rats.
Physiology & behavior, 2009Co-Authors: Jianqun Yan, Xuejuan YangAbstract:Previous studies, which have mostly focused on concentrated NaCl solution intake, have suggested Sodium Depletion may be accompanied with salt taste sensory changes. To further investigate whether the function of the salt taste system changes in different patterns for highly concentrated and diluted NaCl taste stimuli, the effects of Sodium Depletion on NaCl taste detection threshold in rats were examined. After a conditioned taste aversion (CTA) to a suprathreshold concentration of NaCl (0.1 M) was established, rats were given a series of two-bottle choice tests between distilled water and different concentrations of NaCl. Conditioned rats will generalize the aversion to diluted solutions when they are detected. The taste detection threshold for NaCl is defined as the lowest concentration at which there is a reliable difference in the preference scores between conditioned and control subjects. The results showed that detection threshold for NaCl lay between 0.003 M and 0.005 M in Sodium-replete rats, whereas in Sodium-depleted rats that have an amplified action of angiotensin II in the brain, the threshold significantly decreased to be between 0.0001 M and 0.0003 M. However, in rats with a blocked action of angiotensin II in the brain the decreased NaCl detection threshold was between 0.001 M and 0.003 M. These findings suggest that Sodium-depleted rats could decrease the NaCl taste detection threshold to increase the ability to find Sodium ions. And the regulation of the salt taste sensitivity may be related to the action of angiotensin II in brain.
