Early osmoregulatory stimulation of neurohypophyseal  hormone secretion and thirst after gastric NaCl loads

Stricker, Edward M.; Callahan, John B.; Huang, Wan; Sved, Alan F.

doi:10.1152/ajpregu.00548.2001

Cited by 41 publications

(32 citation statements)

References 40 publications

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“…It is important to point out that there was a positive relationship between the number of OT-activated cells and the volume of hypertonic saline consumed, since the animals stimulated to drink, like the PD-2% group, had the greatest number of Fos-OT-ir cells. In accord with these results, there is evidence that intragastric hypertonic infusion enhances OT plasma levels and oxytocin mRNA expression in the hypothalamic nuclei in euhydrated and dehydrated rats, although this peptide does not increase after isotonic intragastric infusion, perhaps because it does not cause substantial hypernatremia or a hypertonic state (20,36,52). Together, these studies suggest that the OT system is a hypertonicity marker; thus the OT circuit may be signaling the entry to the body of a hypertonic sodium solution during sodium access, since 2% NaCl loading or ingestion increases OT neuron activity and OT plasma levels.…”

Section: Effect Of Induced Isotonic Vs Hypertonic Sodium Intake On Pmentioning

confidence: 64%

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Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

Godino¹,

Luca²,

Antunes‐Rodrigues³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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Godino A, De Luca LA, Jr, Antunes-Rodrigues J, Vivas L. Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers? Am J Physiol Regul Integr Comp Physiol 293: R1027-R1036, 2007. First published June 13, 2007; doi:10.1152/ajpregu.00078.2007.-Previous studies demonstrated the inhibitory participation of serotonergic (5-HT) and oxytocinergic (OT) neurons on sodium appetite induced by peritoneal dialysis (PD) in rats. The activity of 5-HT neurons increases after PD-induced 2% NaCl intake and decreases after sodium depletion; however, the activity of the OT neurons appears only after PDinduced 2% NaCl intake. To discriminate whether the differential activations of the 5-HT and OT neurons in this model are a consequence of the sodium satiation process or are the result of stimulation caused by the entry to the body of a hypertonic sodium solution during sodium access, we analyzed the number of Fos-5-HT-and Fos-OTimmunoreactive neurons in the dorsal raphe nucleus and the paraventricular nucleus of the hypothalamus-supraoptic nucleus, respectively, after isotonic vs. hypertonic NaCl intake induced by PD. We also studied the OT plasma levels after PD-induced isotonic or hypertonic NaCl intake. Sodium intake induced by PD significantly increased the number of Fos-5-HT cells, independently of the concentration of NaCl consumed. In contrast, the number of Fos-OT neurons increased after hypertonic NaCl intake, in both depleted and nondepleted animals. The OT plasma levels significantly increased only in the PD-induced 2% NaCl intake group in relation to others, showing a synergic effect of both factors. In summary, 5-HT neurons were activated after body sodium status was reestablished, suggesting that this system is activated under conditions of satiety. In terms of the OT system, both OT neural activity and OT plasma levels were increased by the entry of hypertonic NaCl solution during sodium consumption, suggesting that this system is involved in the processing of hyperosmotic signals. sodium appetite; dorsal raphe nucleus; paraventricular nucleus; supraoptic nucleus; tonicity signals INHIBITORY MECHANISMS OF SODIUM appetite involve oxytocinergic (OT) and serotonergic (5-HT) neurons: hypertonic NaCl intake by sodium-depleted rats activates both groups of neurons as shown, for example, by Fos expression, and increased sodium appetite results when these neurons, their projections, or receptors are inactivated (13,14,29,30,31). However, the inhibitory function of these two systems is not entirely clear. They might be part of a system that prevents cell dehydration by restraining hypertonic solution intake during the expression of sodium appetite in hypovolemic animals, but it is also possible that their activation itself leads to satiety or the termination of sodium appetite.Moreover, each neuronal group may also have its own role within inhibitory systems. For example, sodium depletion and subsequent hypertonic NaCl intake, respectively, decrease and increase Fos expre...

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Section: Effect Of Induced Isotonic Vs Hypertonic Sodium Intake On Pmentioning

confidence: 64%

“…We also studied the neural activity of other brain nuclei previously involved in sodium appetite regulation after PD-induced isotonic or hypertonic NaCl intake and OT plasma levels following the same paradigm, since OT plasma release in other models has been associated with hypernatremic, hyperosmolalic, and hypovolemic stimulation (20,25,52,55).…”

mentioning

confidence: 99%

Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

Godino¹,

Luca²,

Antunes‐Rodrigues³

et al. 2007

American Journal of Physiology-Regulatory, Integrative and Comp

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“…One possible explanation for these studies might be that plasma AVP and Na levels might vary quickly, making it difficult to detect changes. In addition to the central action, it might also be possible that ingested Na stimulated AVP release as well as the sense of thirst through osmoreceptors located in the peripheral tissues (7,27,42). In contrast to the wild-type mice, urine AVP was increased in the 2.0% Na diet group compared with the 0.2% Na group only for 2 mo in the FNDI mice.…”

Section: Discussionmentioning

confidence: 99%

“…In the first experiment, we administered desmopressin (dDAVP), a longacting analog of AVP (13), to the FNDI mouse model to decrease AVP synthesis, and examined possible changes in the phenotype. In the second experiment, we examined whether the excess in Na intake might accelerate the phenotype in the FNDI mice model, as it was demonstrated that the Na intake stimulated AVP release (12,42).…”

mentioning

confidence: 99%

Activation of vasopressin neurons leads to phenotype progression in a mouse model for familial neurohypophysial diabetes insipidus

Hiroi

Morishita

Hayashi

et al. 2010

American Journal of Physiology-Regulatory, Integrative and Comp

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Familial neurohypophysial diabetes insipidus (FNDI) is a rare disease that is inherited in an autosomal dominant manner. In a previous study, we made a mouse model for FNDI, which showed progressive polyuria accompanied by inclusion bodies in the arginine vasopressin (AVP) neurons formed by aggregates in the endoplasmic reticulum. The present study was conducted to determine whether the activities of AVP neurons are related to the phenotype progression in the FNDI model. In the first experiment, female heterozygous mice were administered either desmopressin (dDAVP) or a vehicle (control) subcutaneously with osmotic minipumps for 30 days. The dDAVP treatment significantly decreased the urine volume, AVP mRNA expression, and inclusion bodies in the AVP neurons. Urine volume in the dDAVP group remained significantly less than the control for 14 days even after the minipumps were removed. In the second experiment, the males were fed either a 0.2% Na or 2.0% Na diet for 6 mo. Urine AVP excretion was significantly increased in the 2.0% Na group compared with the 0.2% Na group for the first 2 mo but gradually decreased thereafter. Throughout the experiments, urine volume increased progressively in the 2.0% Na group but not in the 0.2% Na group. Immunohistochemical analyses revealed that inclusion bodies in the AVP cells had significantly increased in the 2.0% Na compared with the 0.2% Na group. These data demonstrated that activation of AVP neurons could accelerate the aggregate formation as well as the progression of the polyuria in the FNDI model mice.hereditary disease; aggregates ARGININE VASOPRESSIN (AVP), an antidiuretic hormone, is synthesized in the magnocellular neurons of the supraoptic nucleus (SON) and paraventricular nucleus of the hypothalamus (2, 36). The synthesis, as well as the release of AVP, is stimulated by increases in plasma osmolality and decreases in blood volume (blood pressure) (2, 36). The process from synthesis to release includes transcription, translation of the mRNA, folding of the precursor within the endoplasmic reticulum (ER), cleavage of the precursors during axonal transport, and release of AVP into the circulation (6).AVP plays a pivotal role in the homeostasis of water balance, and a deficiency of AVP leads to diabetes insipidus (DI) characterized by polyuria (22). Familial neurohypophysial DI (FNDI) is a rare autosomal dominant disorder (23). More than 50 point mutations in FNDI have been reported in the AVP gene so far, with most mutations existing in the domain of neurophysin II (NPII) (11), which functions as a carrier protein of AVP (36). While mechanisms underlying progressive polyuria in FNDI have not yet been fully elucidated, we demonstrated recently (15) that aggregates had progressively accumulated in the ER of AVP neurons in parallel with the progressive polyuria in mice possessing a point mutation (Cys98stop) in the NPII gene, which causes FNDI in humans (26). These data suggest that the accumulations of aggregates in ER that were probably derived from AVP precursors ...

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“…Typically as P osm increases, plasma arginine vasopressin and thirst increase. This relationship has been illustrated in numerous studies (Greenleaf 1992;O'Brien et al 1998;Phillips et al 1985;Stricker et al 2002;Thompson et al 1986). However, changes in central volume have been shown to alter this relationship between thirst and P osm .…”

Section: Discussionmentioning

confidence: 77%

Effect of increased plasma osmolality on cold-induced thirst attenuation

et al. 2008

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The eVects of elevating plasma osmolality (P osm ) on thirst ratings was studied in eight dehydrated males during exposure to 4°C. On two occasions, subjects were dehydrated (DH; 3-4% body mass) via 90 min exercise-heat exposure and overnight Xuid restriction (day 1). On a third occasion, subjects were exposed to heat but were given Xuid (EU). On day 2, subjects consumed NaCl (NaCl; 0.1 g NaCl kg ¡1 body mass in 500 ml H 2 O; DH only) or Placebo (P; 500 ml H 2 O; DH and EU). Subjects stood for 30 min at 24°C and for 45 min at 4°C (75 min post-dose). P osm was elevated (P < 0.05) 30 and 75 min after NaCl administration in DH + NaCl versus DH + P and EU + P treatments. Thirst ratings remained elevated (P < 0.05) in the DH + NaCl treatment 30 min after dosing and 45 min at 4°C versus DH + P and EU + P. Attenuation of thirst when dehydrated in the cold can be over-ridden by increasing P osm .

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Early osmoregulatory stimulation of neurohypophyseal hormone secretion and thirst after gastric NaCl loads

Cited by 41 publications

References 40 publications

Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

Oxytocinergic and serotonergic systems involvement in sodium intake regulation: satiety or hypertonicity markers?

Activation of vasopressin neurons leads to phenotype progression in a mouse model for familial neurohypophysial diabetes insipidus

Effect of increased plasma osmolality on cold-induced thirst attenuation

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