Osmoreceptors, Osmoreception, and Osmoregulation

Bourque, Charles W.; Oliet, Stéphane H. R.; Richard, Dominique

doi:10.1006/frne.1994.1010

Cited by 296 publications

(244 citation statements)

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“…Small changes in plasma osmolality in the physiological range can rapidly stimulate AVP transcription in the SON and PVN, suggesting that stored AVP released into the blood circulation is replaced rapidly by increased synthesis, processing, and transport of AVP (12). The threshold for the activation of osmoreceptor neurons to stimulate AVP release is approximately 275 mOsm/kg (13). In addition, lesions of the AV3V cause adipsia and hypernatremia (2), impaired drinking responses and AVP secretion in response to hypertonic saline and angiotensin II (14), decrease of the number of Fos-like immunoreactive neurons in the MnPO, PVN and SON in response to iv infusion of hypertonic saline (15), and interruption of neuronal inputs that trigger AVP secretion from the posterior pituitary as well as AVP release into the extracellular compartment of the SON (16).…”

Section: Neurohypophyseal Hormones and The Control Of Sodium And Watementioning

confidence: 99%

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Ventura

Gomes

Reis

et al. 2002

Braz J Med Biol Res

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The central nervous system plays an important role in the control of renal sodium excretion. We present here a brief review of physiologic regulation of hydromineral balance and discuss recent results from our laboratory that focus on the participation of nitrergic, vasopressinergic, and oxytocinergic systems in the regulation of water and sodium excretion under different salt intake and hypertonic blood volume expansion (BVE) conditions. High sodium intake induced a significant increase in nitric oxide synthase (NOS) activity in the medial basal hypothalamus and neural lobe, while a low sodium diet decreased NOS activity in the neural lobe, suggesting that central NOS is involved in the control of sodium balance. An increase in plasma concentrations in vasopressin (AVP), oxytocin (OT), atrial natriuretic peptide (ANP), and nitrate after hypertonic BVE was also demonstrated. The central inhibition of NOS by L-NAME caused a decrease in plasma AVP and no change in plasma OT or ANP levels after BVE. These data indicate that the increase in AVP release after hypertonic BVE depends on nitric oxide production. In contrast, the pattern of OT secretion was similar to that of ANP secretion, supporting the view that OT is a neuromodulator of ANP secretion during hypertonic BVE. Thus, neurohypophyseal hormones and ANP are secreted under hypertonic BVE in order to correct the changes induced in blood volume and osmolality, and the secretion of AVP in this particular situation depends on NOS activity. Central nervous system and hydromineral balancePrecise regulation of body fluid osmolality is essential. Osmolality is controlled by a finely tuned, intricate homeostatic mechanism that operates by adjusting both the rate of water intake and excretion. The central nervous system (CNS) plays an important role in the control of renal sodium excretion (1-7). Considerable evidence indicates that the median preoptic area (MnPO), anterior lateral hypothalamus, subfornical organ (SFO), anterior portion of the third ventricle (AV3V), supraoptic nucleus (SON), paraventricular nucleus (PVN), organum vasculosum laminae terminalis (OVLT), habenula, stria medullaris, and medial septal area are organized in a neural circuit involved in the regulation of water and sodium intake and excretion (1-3). Natriuresis accompanied by kaliuresis is induced by cholinergic or adrenergic stimulation of the medial septal area, MnPO, anterior lateral hypothalamus, SFO, and AV3V (1,4). Stimulation of AV3V with carbachol, a cholinergic drug, angiotensin II or hypertonic saline enhances natriuresis, which is blocked by the destruction of this brain area (1,4-7). Neurohypophyseal hormones and the control of sodium and water excretionAlthough the neuroendocrine control of sodium and water balance is not completely understood, alterations in volume and osmolality are responsible, at least in part, for changes in plasma vasopressin (AVP) concentration. Verney (8) originally demonstrated that AVP release into the blood is stimulated by the activation of os...

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Section: Neurohypophyseal Hormones and The Control Of Sodium And Watementioning

confidence: 99%

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Ventura

Gomes

Reis

et al. 2002

Braz J Med Biol Res

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“…It is well established that the production of vasopressin varies in accordance with changes in the osmotic pressure of the plasma as hypertonic stimuli enhance, whereas hypotonic stimuli decrease the synthesis and release of VP (1,17). The importance of astrocytes in regulating hypotonicity has been well documented (2,18), while the mechanism by which astrocytes regulate hypertonicity remains to be elucidated.…”

Section: Discussionmentioning

confidence: 99%

“…The maintenance of stable osmolarity in the extracellular fluid is essential for physiological functioning and is partly achieved via the regulation of vasopressin (VP) release from the neurohypophysial axon terminals of the magnocellular neurosecretory cells (MNCs) in the supraoptic nucleus (SON) and the paraventricular nucleus (PVN) (1). Several studies demonstrated that astrocytes in the SON and PVN also have important roles in regulating osmotic pressure (2).…”

Section: Introductionmentioning

confidence: 99%

Involvement of connexin43 in the acute hyperosmotic stimulus-induced synthesis and release of vasopressin in the supraoptic nucleus of rats

Jiang

Wang

et al. 2014

Molecular Medicine Reports

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Abstract. There is evidence that astroglial connexin43 (Cx43) in the supraoptic nucleus (SON) is required for the hyperosmolarity-induced increase in Fos protein expression in magnocellular neurosecretory cells (MNCs). In the present study, the role of astroglial Cx43 in the synthesis and release of vasopressin (VP) by MNCs in the SON subjected to hyperosmotic stimulus was examined. The results revealed that the VP levels in the SON and plasma were increased following acute hyperosmotic stimulus. Treatment of MNCs with Cx43-specific antisense oligodeoxynucleotides (ASODN), which temporarily reduced Cx43 protein production, limited the VP synthesis and release induced by a hyperosmotic stimulus. Similarly, the addition of gap junction and Cx43 hemichannel blockers also attenuated the VP synthesis and release induced by an acute hyperosmotic stimulus. A high extracellular [Ca 2+ ]( [Ca 2+ ] o ) has been demonstrated to reduce the gap junction activity or opening probability of Cx54 hemichannels. Notably, it was identified that high [Ca 2+ ] o attenuated the VP synthesis and release induced by acute hyperosmotic stimulus, while low [Ca 2+ ] o had a weak or no effect. These results suggested that Cx43 participates in the VP synthesis and release induced by hyperosmotic stimulation in the SON.

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“…By providing him with water during school sessions ostensibly to keep him alert, his teachers inadvertently treated his osmoregulatory dysfunction, which only came to light after he was on school break. The organum vasculosum of the lamina terminalis and subfornical organ are established key areas for thirst perception, fluid-seeking behavior, osmoregulation, and vasopressin secretion [22]. Experimental models with ablative lesions of the subfornical organ display adipsia or hypodipsia [23], and those with lesions of the lamina terminalis and region anteroventral to the third ventricle have impaired response to osmotic stimulation and impaired vasopressin secretion [24].…”

Section: Discussionmentioning

confidence: 99%

Central diabetes insipidus and adipsia due to astrocytoma: diagnosis and management

2012

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Adipsia and/or diabetes insipidus is rarely a direct complication of astrocytoma. We report a young man with recurrence of anaplastic astrocytoma who presented as severe hypernatremia. This case highlights key diagnostic and therapeutic challenges: (1) the interpretation of the response to exogenous vasopressin in a patient with steroid-induced hyperglycemia and (2) the potential risk of brain edema and herniation if excess water is prescribed along with vasopressin supplementation. The patient was successfully managed with prescribed fluid replacement, daily weights, and regular electrolyte monitoring but no exogenous vasopressin for 8 months until he succumbed to his tumor.

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Osmoreceptors, Osmoreception, and Osmoregulation

Cited by 296 publications

References 0 publications

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Involvement of connexin43 in the acute hyperosmotic stimulus-induced synthesis and release of vasopressin in the supraoptic nucleus of rats

Central diabetes insipidus and adipsia due to astrocytoma: diagnosis and management

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