The Experts below are selected from a list of 11994 Experts worldwide ranked by ideXlab platform
Jennifer S. Pollock - One of the best experts on this subject based on the ideXlab platform.
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collecting duct nitric oxide synthase 1s activation maintains Sodium Homeostasis during high Sodium intake through suppression of aldosterone and renal angiotensin ii pathways
Journal of the American Heart Association, 2017Co-Authors: Kelly A. Hyndman, Elena Mironova, Jorge F. Giani, Courtney Dugas, Jessika Collins, Alicia A. Mcdonough, James D. Stockand, Jennifer S. PollockAbstract:BackgroundDuring high Sodium intake, the renin‐angiotensin‐aldosterone system is downregulated and nitric oxide signaling is upregulated in order to remain in Sodium balance. Recently, we showed th...
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nitric oxide and the a and b of endothelin of Sodium Homeostasis
Current Opinion in Nephrology and Hypertension, 2013Co-Authors: Kelly A. Hyndman, Jennifer S. PollockAbstract:PURPOSE OF REVIEW In recent years, renal collecting duct-specific endothelin-1 (ET1), endothelin A (ETA) and endothelin B (ETB) receptors as well as nitric oxide synthase 1 (NOS1) knockout mice have been developed with subsequent identification for an integral role in regulation of Sodium water Homeostasis and ultimately blood pressure. The focus of this review is to integrate these models and to propose a scheme for the control of Sodium excretion by the collecting duct and the endothelin/ETB/NOS system. RECENT FINDINGS NOS1 splice variants are expressed in the kidney, especially in the collecting duct. Mice express predominantly NOS1β in the medulla, with NOS1α and NOS1β in the cortex, whereas rats express NOS1α and NOS1β in both the cortex and medulla. Novel transcription of collecting duct ET1 mediated by epithelial Sodium channels, mitochondrial Na/Ca exchangers and glucocorticoids has been determined. ET1 via the ETB receptor increases nitric oxide production in both rat and mouse collecting ducts, suggesting that NOS1β is linked to ET1-dependent NOS activation in the kidney. As well, genetic deletion of NOS1 splice variants in the collecting duct results in a salt-sensitive hypertensive phenotype in mice, much like the collecting duct ET1 and collecting duct ETB knockout mice. SUMMARY In the collecting duct, the ET1/nitric oxide pathways are intimately linked, and deletion of collecting duct ET1, ETB receptor or NOS1β results in a salt-sensitive phenotype, which is at least partially dependent on dysregulation of Sodium and water reabsorption.
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endothelin and nos1 nitric oxide signaling and regulation of Sodium Homeostasis
Current Opinion in Nephrology and Hypertension, 2008Co-Authors: Jennifer S. Pollock, David M PollockAbstract:Purpose of reviewIn general, the nitric oxide and endothelin signaling pathways in the kidney promote natriuresis. The basis for this statement will first be reviewed for each of these systems. Next, this review will outline the progression of data providing support for our hypothesis that an intra-
Robin A. Felder - One of the best experts on this subject based on the ideXlab platform.
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The Renal Sodium Bicarbonate Cotransporter NBCe2: Is It a Major Contributor to Sodium and pH Homeostasis?
Current Hypertension Reports, 2016Co-Authors: Robin A. Felder, Pedro A. Jose, John J. GildeaAbstract:The Sodium bicarbonate cotransporter (NBCe2, aka NBC4) was originally isolated from the human testis and heart (Pushkin et al. IUBMB Life 50:13–19, 2000 ). Subsequently, NBCe2 was found in diverse locations where it plays a role in regulating Sodium and bicarbonate transport, influencing intracellular, extracellular, interstitial, and ultimately plasma pH (Boron et al. J Exp Biol. 212:1697–1706, 2009 ; Parker and Boron, Physiol Rev. 93:803–959, 2013 ; Romero et al. Mol Asp Med. 34:159–182, 2013 ). NBCe2 is located in human and rodent renal-collecting duct and proximal tubule. While much is known about the two electrogenic Sodium bicarbonate cotransporters, NBCe1 and NBCe2, in the regulation of Sodium Homeostasis and pH balance in the rodent kidney, little is known about their roles in human renal physiology. NBCe2 is located in the proximal tubule Golgi apparatus under basal conditions and then disperses throughout the cell, but particularly into the apical membrane microvilli, during various maneuvers that increase intracellular Sodium. This review will summarize our current understanding of the distribution and function of NBCe2 in the human kidney and how genetic variants of its gene, SLC4A5 , contribute to salt sensitivity of blood pressure.
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the importance of the gastrorenal axis in the control of body Sodium Homeostasis
Experimental Physiology, 2016Co-Authors: Pedro A. Jose, Zhiwei Yang, Chunyu Zeng, Robin A. FelderAbstract:What is the topic of this review? Sensing the amount of ingested Sodium is one mechanism by which Sodium balance is regulated. This review describes the role of gastrin in the cross-talk between the stomach and the kidney following the ingestion of Sodium. What advances does it highlight? Neural mechanisms and several gut hormones, including cholecystokinin and uroguanylin, have been suggested to mediate the natriuresis after an oral Sodium load. It is proposed that gastrin produced by G-cells via its receptor, cholecystokinin B receptor, interacts with renal D1 -like dopamine receptors to increase renal Sodium excretion. Hypertension develops with chronically increased Sodium intake when Sodium that accumulates in the body can no longer be sequestered, extracellular fluid volume is expanded, and compensatory neural, hormonal and pressure-natriuresis mechanisms fail. Sensing the amount of ingested Sodium, by the stomach, is one mechanism by which Sodium balance is regulated. The natriuresis following the ingestion of a certain amount of Sodium may be due to an enterokine, gastrin, secreted by G-cells in the stomach and duodenum and released into the circulation. Circulating gastrin levels are 10- to 20-fold higher than those for cholecystokinin. Of all the gut hormones circulating in the plasma, gastrin is the one that is reabsorbed to the greatest extent by renal tubules. Gastrin, via its receptor, the cholecystokinin type B receptor (CCKBR), is natriuretic in mammals, including humans, by inhibition of renal Sodium transport. Germline deletion of gastrin (Gast) or Cckbr gene in mice causes salt-sensitive hypertension. Selective silencing of Gast in the stomach and duodenum impairs the ability to excrete an oral Sodium load and also increases blood pressure. Thus, the gastrorenal axis, mediated by gastrin, can complement pronatriuretic hormones, such as dopamine, to increase Sodium excretion after an oral Sodium load. These studies in mice may be translatable to humans because the chromosomal loci of CCKBR and GAST are linked to human essential hypertension. Understanding the role of genes in the regulation of renal function and blood pressure may lead to the tailoring of antihypertensive treatment based on genetic make-up.
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renal dopamine and Sodium Homeostasis
Current Hypertension Reports, 2000Co-Authors: Pedro A. Jose, Gilbert M Eisner, Robin A. FelderAbstract:During the past decade, it has become evident that dopamine plays an important role in the regulation of fluid and electrolyte balance and blood pressure. Dopamine exerts its actions through two families of dopamine receptors, designated D1-like and D2-like, which are identical in the brain and in peripheral tissues. The two D1-like receptors--D1 and D5 receptors--expressed in mammals are linked to stimulation of adenylyl cyclase. The three D2-like receptors--D2, D3, and D4,--are linked to inhibition of adenylyl cyclase. Dopamine affects fluid and electrolyte balance by regulation of renal excretion of electrolytes and water through actions on renal hemodynamics and tubular epithelial transport and by modulation of the secretion and/or action of vasopressin, renin, aldosterone, catecholamines, and endothelin B receptors (ETB) receptors. It also affects fluid and Sodium intake by way of "appetite" centers in the brain and alterations of gastrointestinal tract transport. The production of dopamine in neural and non-neural tissues and the presence of receptors in these tissues suggest that dopamine can act in an autocrine or paracrine fashion. This renal autocrine-paracrine function, which becomes most evident during extracellular fluid volume expansion, is lost in essential hypertension and in some animal models of genetic hypertension. This deficit may be caused by abnormalities in renal dopamine production and polymorphisms or abnormal post-translational modification and regulation of dopamine receptor subtypes.
Michael G Harrington - One of the best experts on this subject based on the ideXlab platform.
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regulation of csf and brain tissue Sodium levels by the blood csf and blood brain barriers during migraine
Frontiers in Computational Neuroscience, 2020Co-Authors: Hamed Ghaffari, Samuel C Grant, Linda R Petzold, Michael G HarringtonAbstract:Author(s): Ghaffari, Hamed; Grant, Samuel C; Petzold, Linda R; Harrington, Michael G | Abstract: Cerebrospinal fluid (CSF) and brain tissue Sodium levels increase during migraine. However, little is known regarding the underlying mechanisms of Sodium Homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of Sodium dysregulation in the brain is important, since correction of the altered Sodium Homeostasis could potentially treat migraine. Under the hypothesis that disturbances in Sodium transport mechanisms at the blood-CSF barrier (BCSFB) and/or the blood-brain barrier (BBB) are the underlying cause of the elevated CSF and brain tissue Sodium levels during migraines, we developed a mechanistic, differential equation model of a rat's brain to compare the significance of the BCSFB and the BBB in controlling CSF and brain tissue Sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue and blood. Sodium transport from blood to CSF across the BCSFB, and from blood to brain tissue across the BBB were modeled by influx permeability coefficients P BCSFB and P BBB , respectively, while Sodium movement from CSF into blood across the BCSFB, and from brain tissue to blood across the BBB were modeled by efflux permeability coefficients PBCSFB' and PBBB' , respectively. We then performed a global sensitivity analysis to investigate the sensitivity of the ventricular CSF, subarachnoid CSF and brain tissue Sodium concentrations to pathophysiological variations in P BCSFB , P BBB , PBCSFB' and PBBB' . Our results show that the ventricular CSF Sodium concentration is highly influenced by perturbations of P BCSFB , and to a much lesser extent by perturbations of PBCSFB' . Brain tissue and subarachnoid CSF Sodium concentrations are more sensitive to pathophysiological variations of P BBB and PBBB' than variations of P BCSFB and PBCSFB' within 30 min of the onset of the perturbations. However, P BCSFB is the most sensitive model parameter, followed by P BBB and PBBB' , in controlling brain tissue and subarachnoid CSF Sodium levels within 3 h of the perturbation onset.
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regulation of csf and brain tissue Sodium levels by the blood csf and blood brain barriers during migraine
bioRxiv, 2019Co-Authors: Hamed Ghaffari, Samuel C Grant, Linda R Petzold, Michael G HarringtonAbstract:Background: It is known that Sodium concentration in both cerebrospinal fluid (CSF) and brain interstitial fluid (ISF) increases during migraine. However, little is known regarding the underlying mechanisms of Sodium Homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of Sodium dysregulation in the brain is important, since correction of the altered Sodium Homeostasis could potentially treat migraine. Methods: Under the hypothesis that disturbed Homeostasis of brain capillary endothelial cells (CEC) and choroid plexus (CP) Sodium-potassium pump (SPP) is the underlying cause of the elevated CSF and ISF Sodium levels in migraine sufferers, we developed a mechanistic, differential equation model of a rat brain to compare the significance of CP and CEC SPPs in controlling CSF and ISF Sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue, plasma and CP. The activity levels of CP and CEC SPPs are modeled by permeability coefficients of CP and CEC to Sodium, respectively. We then performed a global sensitivity analysis to investigate the significance of CEC and CP permeabilities to Sodium in controlling CSF and ISF Sodium concentrations. Results: We show that the variation of permeability of CP to Sodium is much more important than the alteration of CEC permeability to Sodium in controlling CSF and ISF Sodium levels. Our simulations indicate that the Sodium flux at the interface of the ventricular system and brain tissue is greater than the Sodium flux at the contact surface of the brain tissue and subarachnoid space during an episode of migraine. Conclusions: Using mathematical modeling, we demonstrate that overactivity of CP SPPs has a more significant effect than overactivity of CEC SPPs on ISF and CSF Sodium concentrations. Our results suggest that altered Homeostasis of CP SPPs is a potential cause of migraines in the rats. Further studies on CP SPP activity levels during migraine episodes with different triggers can help better understand migraine pathophysiology.
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regulation of cerebrospinal fluid and brain tissue Sodium levels by choroid plexus and brain capillary endothelial cell na k atpases during migraine
bioRxiv, 2019Co-Authors: Hamed Ghaffari, Samuel C Grant, Linda R Petzold, Michael G HarringtonAbstract:BackgroundIt is known that Sodium concentration in both cerebrospinal fluid (CSF) and brain interstitial fluid (ISF) increases during migraine. However, little is known regarding the underlying mechanisms of Sodium Homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of Sodium dysregulation in the brain is important, since correction of the altered Sodium Homeostasis could potentially treat migraine.nnMethodsUnder the hypothesis that disturbed Homeostasis of brain capillary endothelial cells (CEC) and choroid plexus (CP) Sodium-potassium pump (SPP) is the underlying cause of the elevated CSF and ISF Sodium levels in migraine sufferers, we developed a mechanistic, differential equation model of a rats brain to compare the significance of CP and CEC SPPs in controlling CSF and ISF Sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue, plasma and CP. The activity levels of CP and CEC SPPs are modeled by permeability coefficients of CP and CEC to Sodium, respectively. We then performed a global sensitivity analysis to investigate the significance of CEC and CP permeabilities to Sodium in controlling CSF and ISF Sodium concentrations.nnResultsWe show that the variation of permeability of CP to Sodium is much more important than the alteration of CEC permeability to Sodium in controlling CSF and ISF Sodium levels. Our simulations indicate that the Sodium flux at the interface of the ventricular system and brain tissue is greater than the Sodium flux at the contact surface of the brain tissue and subarachnoid space during an episode of migraine.nnConclusionsUsing mathematical modeling, we demonstrate that overactivity of CP SPPs has a more significant effect than overactivity of CEC SPPs on ISF and CSF Sodium concentrations. Our results suggest that altered Homeostasis of CP SPPs is a potential cause of migraines in the rats. Further studies on CP SPP activity levels during migraine episodes with different triggers can help better understand migraine pathophysiology.
Robert M. Carey - One of the best experts on this subject based on the ideXlab platform.
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theodore cooper lecture renal dopamine system paracrine regulator of Sodium Homeostasis and blood pressure
Hypertension, 2001Co-Authors: Robert M. CareyAbstract:All of the components of a complete dopamine system are present within the kidney, where dopamine acts as a paracrine substance in the control of Sodium excretion. Dopamine receptors can be divided into D(1)-like (D(1) and D(5)) receptors that stimulate adenylyl cyclase and D(2)-like (D(2), D(3), and D(4)) receptors that inhibit adenylyl cyclase. All 5 receptor subtypes are expressed in the kidney, albeit in low copy. Dopamine is synthesized extraneuronally in proximal tubule cells, exported from these cells largely into the tubule lumen, and interacts with D(1)-like receptors to inhibit the Na(+)-H(+) exchanger and Na(+),K(+)-ATPase, decreasing tubule Sodium reabsorption. During moderate Sodium surfeit, dopamine tone at D(1)-like receptors accounts for approximately 50% of Sodium excretion. In experimental and human hypertension, 2 renal dopaminergic defects have been described: (1) decreased renal generation of dopamine and (2) a D(1) receptor-G protein coupling defect. Both defects lead to renal Sodium retention, and each may play an important role in the pathophysiology of essential hypertension.
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Renal Dopamine System: Paracrine Regulator of Sodium Homeostasis and Blood Pressure
Hypertension, 2001Co-Authors: Robert M. CareyAbstract:All of the components of a complete dopamine system are present within the kidney, where dopamine acts as a paracrine substance in the control of Sodium excretion. Dopamine receptors can be divided into D 1 -like (D 1 and D 5 ) receptors that stimulate adenylyl cyclase and D 2 -like (D 2 , D 3 , and D 4 ) receptors that inhibit adenylyl cyclase. All 5 receptor subtypes are expressed in the kidney, albeit in low copy. Dopamine is synthesized extraneuronally in proximal tubule cells, exported from these cells largely into the tubule lumen, and interacts with D 1 -like receptors to inhibit the Na + -H + exchanger and Na + ,K + -ATPase, decreasing tubule Sodium reabsorption. During moderate Sodium surfeit, dopamine tone at D 1 -like receptors accounts for ≈50% of Sodium excretion. In experimental and human hypertension, 2 renal dopaminergic defects have been described: (1) decreased renal generation of dopamine and (2) a D 1 receptor-G protein coupling defect. Both defects lead to renal Sodium retention, and each may play an important role in the pathophysiology of essential hypertension.
Hamed Ghaffari - One of the best experts on this subject based on the ideXlab platform.
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regulation of csf and brain tissue Sodium levels by the blood csf and blood brain barriers during migraine
Frontiers in Computational Neuroscience, 2020Co-Authors: Hamed Ghaffari, Samuel C Grant, Linda R Petzold, Michael G HarringtonAbstract:Author(s): Ghaffari, Hamed; Grant, Samuel C; Petzold, Linda R; Harrington, Michael G | Abstract: Cerebrospinal fluid (CSF) and brain tissue Sodium levels increase during migraine. However, little is known regarding the underlying mechanisms of Sodium Homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of Sodium dysregulation in the brain is important, since correction of the altered Sodium Homeostasis could potentially treat migraine. Under the hypothesis that disturbances in Sodium transport mechanisms at the blood-CSF barrier (BCSFB) and/or the blood-brain barrier (BBB) are the underlying cause of the elevated CSF and brain tissue Sodium levels during migraines, we developed a mechanistic, differential equation model of a rat's brain to compare the significance of the BCSFB and the BBB in controlling CSF and brain tissue Sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue and blood. Sodium transport from blood to CSF across the BCSFB, and from blood to brain tissue across the BBB were modeled by influx permeability coefficients P BCSFB and P BBB , respectively, while Sodium movement from CSF into blood across the BCSFB, and from brain tissue to blood across the BBB were modeled by efflux permeability coefficients PBCSFB' and PBBB' , respectively. We then performed a global sensitivity analysis to investigate the sensitivity of the ventricular CSF, subarachnoid CSF and brain tissue Sodium concentrations to pathophysiological variations in P BCSFB , P BBB , PBCSFB' and PBBB' . Our results show that the ventricular CSF Sodium concentration is highly influenced by perturbations of P BCSFB , and to a much lesser extent by perturbations of PBCSFB' . Brain tissue and subarachnoid CSF Sodium concentrations are more sensitive to pathophysiological variations of P BBB and PBBB' than variations of P BCSFB and PBCSFB' within 30 min of the onset of the perturbations. However, P BCSFB is the most sensitive model parameter, followed by P BBB and PBBB' , in controlling brain tissue and subarachnoid CSF Sodium levels within 3 h of the perturbation onset.
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regulation of csf and brain tissue Sodium levels by the blood csf and blood brain barriers during migraine
bioRxiv, 2019Co-Authors: Hamed Ghaffari, Samuel C Grant, Linda R Petzold, Michael G HarringtonAbstract:Background: It is known that Sodium concentration in both cerebrospinal fluid (CSF) and brain interstitial fluid (ISF) increases during migraine. However, little is known regarding the underlying mechanisms of Sodium Homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of Sodium dysregulation in the brain is important, since correction of the altered Sodium Homeostasis could potentially treat migraine. Methods: Under the hypothesis that disturbed Homeostasis of brain capillary endothelial cells (CEC) and choroid plexus (CP) Sodium-potassium pump (SPP) is the underlying cause of the elevated CSF and ISF Sodium levels in migraine sufferers, we developed a mechanistic, differential equation model of a rat brain to compare the significance of CP and CEC SPPs in controlling CSF and ISF Sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue, plasma and CP. The activity levels of CP and CEC SPPs are modeled by permeability coefficients of CP and CEC to Sodium, respectively. We then performed a global sensitivity analysis to investigate the significance of CEC and CP permeabilities to Sodium in controlling CSF and ISF Sodium concentrations. Results: We show that the variation of permeability of CP to Sodium is much more important than the alteration of CEC permeability to Sodium in controlling CSF and ISF Sodium levels. Our simulations indicate that the Sodium flux at the interface of the ventricular system and brain tissue is greater than the Sodium flux at the contact surface of the brain tissue and subarachnoid space during an episode of migraine. Conclusions: Using mathematical modeling, we demonstrate that overactivity of CP SPPs has a more significant effect than overactivity of CEC SPPs on ISF and CSF Sodium concentrations. Our results suggest that altered Homeostasis of CP SPPs is a potential cause of migraines in the rats. Further studies on CP SPP activity levels during migraine episodes with different triggers can help better understand migraine pathophysiology.
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regulation of cerebrospinal fluid and brain tissue Sodium levels by choroid plexus and brain capillary endothelial cell na k atpases during migraine
bioRxiv, 2019Co-Authors: Hamed Ghaffari, Samuel C Grant, Linda R Petzold, Michael G HarringtonAbstract:BackgroundIt is known that Sodium concentration in both cerebrospinal fluid (CSF) and brain interstitial fluid (ISF) increases during migraine. However, little is known regarding the underlying mechanisms of Sodium Homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of Sodium dysregulation in the brain is important, since correction of the altered Sodium Homeostasis could potentially treat migraine.nnMethodsUnder the hypothesis that disturbed Homeostasis of brain capillary endothelial cells (CEC) and choroid plexus (CP) Sodium-potassium pump (SPP) is the underlying cause of the elevated CSF and ISF Sodium levels in migraine sufferers, we developed a mechanistic, differential equation model of a rats brain to compare the significance of CP and CEC SPPs in controlling CSF and ISF Sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue, plasma and CP. The activity levels of CP and CEC SPPs are modeled by permeability coefficients of CP and CEC to Sodium, respectively. We then performed a global sensitivity analysis to investigate the significance of CEC and CP permeabilities to Sodium in controlling CSF and ISF Sodium concentrations.nnResultsWe show that the variation of permeability of CP to Sodium is much more important than the alteration of CEC permeability to Sodium in controlling CSF and ISF Sodium levels. Our simulations indicate that the Sodium flux at the interface of the ventricular system and brain tissue is greater than the Sodium flux at the contact surface of the brain tissue and subarachnoid space during an episode of migraine.nnConclusionsUsing mathematical modeling, we demonstrate that overactivity of CP SPPs has a more significant effect than overactivity of CEC SPPs on ISF and CSF Sodium concentrations. Our results suggest that altered Homeostasis of CP SPPs is a potential cause of migraines in the rats. Further studies on CP SPP activity levels during migraine episodes with different triggers can help better understand migraine pathophysiology.
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regulation of cerebrospinal fluid and brain tissue Sodium levels by choroid plexus and brain capillary endothelial cell na k atpases during migraine
bioRxiv, 2019Co-Authors: Hamed Ghaffari, Samuel C Grant, Linda R Petzold, Michael HarringtonAbstract:Abstract Background It is known that Sodium concentration in both cerebrospinal fluid (CSF) and brain interstitial fluid (ISF) increases during migraine. However, little is known regarding the underlying mechanisms of Sodium Homeostasis disturbance in the brain during the onset and propagation of migraine. Exploring the cause of Sodium dysregulation in the brain is important, since correction of the altered Sodium Homeostasis could potentially treat migraine. Methods Under the hypothesis that disturbed Homeostasis of brain capillary endothelial cells (CEC) and choroid plexus (CP) Na+, K+-ATPase (NKAT) is the underlying cause of the elevated CSF and ISF Sodium levels in migraine sufferers, we developed a mechanistic, differential equation model of a rat’s brain to compare the significance of CP and CEC NKATs in controlling CSF and ISF Sodium levels. The model includes the ventricular system, subarachnoid space, brain tissue, plasma and CP. The activity levels of CP and CEC NKATs are modeled by permeability coefficients of CP and CEC to Sodium, respectively. We then performed a global sensitivity analysis to investigate the significance of CEC and CP permeabilities to Sodium in controlling CSF and ISF Sodium concentrations. Results We show that the variation of permeability of CP to Sodium is much more important than the alteration of CEC permeability to Sodium in controlling CSF and ISF Sodium levels. Our simulations indicate that the Sodium flux at the interface of the ventricular system and brain tissue is greater than the Sodium flux at the contact surface of the brain tissue and subarachnoid space during an episode of migraine. Conclusions Using mathematical modeling, we demonstrate that overactivity of CP NKATs has a more significant effect than overactivity of CEC NKATs on ISF and CSF Sodium concentrations. Our results suggest that altered Homeostasis of CP NKATs is a potential cause of migraines in the rats. Further studies on CP NKAT activity levels during migraine episodes with different triggers can help better understand migraine pathophysiology.
