WordNet

a silvery soft waxy metallic element of the alkali metal group; occurs abundantly in natural compounds (especially in salt water); burns with a yellow flame and reacts violently in water; occurs in sea water and in the mineral halite (rock salt) (同)Na, atomic number 11
a nonmetallic univalent element that is normally a colorless and odorless highly flammable diatomic gas; the simplest and lightest and most abundant element in the universe (同)H, atomic number 1

PrepTutorEJDIC

ソジウム,ナトリウム(金属元素;化学記号はNa)
『水素』(化学記号は『H』)

Wikipedia preview

出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2012/07/09 21:43:49」(JST)

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The sodium–hydrogen antiporter or sodium–hydrogen exchanger is a membrane protein found in many cells, and especially in those of the nephron of the kidney. It is primarily responsible for maintaining the balance of sodium.^[1]

Isoforms

There are several isoforms of the antiporter:

Sodium–hydrogen antiporter 1
Sodium–hydrogen antiporter 2
Sodium–hydrogen antiporter 3
Sodium–hydrogen antiporter 5
Sodium–hydrogen antiporter 6
Sodium–hydrogen antiporter 8

References

^ VI. Mechanisms of Salt & Water Reabsorption

External links

Sodium-Hydrogen+Exchanger at the US National Library of Medicine Medical Subject Headings (MeSH)

This membrane protein-related article is a stub. You can help Wikipedia by expanding it.

UpToDate Contents

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1. 赤血球水分量の制御 control of red blood cell hydration
2. 幼児および小児における尿細管性アシドーシスの病因および臨床症状 etiology and clinical manifestations of renal tubular acidosis in infants and children
3. 心臓の虚血性再潅流障害 ischemic reperfusion injury of the heart
4. 塩分摂取量および塩分摂取量制限と原発性（本態性）高血圧 salt intake salt restriction and primary essential hypertension
5. 低リン血症の原因 causes of hypophosphatemia

English Journal

Fructose stimulates Na/H exchange activity and sensitizes the proximal tubule to angiotensin II.

Cabral PD1, Hong NJ, Hye Khan MA, Ortiz PA, Beierwaltes WH, Imig JD, Garvin JL.Author information 1Department of Physiology and Biophysics, Case Western Reserve University, 10900 Euclid Ave, Cleveland, OH 44106-4970. pxc273@case.edu.AbstractThe proximal nephron reabsorbs 60% to 70% of the fluid and sodium and most of the filtered bicarbonate via Na/H exchanger 3. Enhanced proximal nephron transport is implicated in hypertension. Our findings show that a fructose-enriched diet causes salt sensitivity. We hypothesized that fructose stimulates luminal Na/H exchange activity and sensitizes the proximal tubule to angiotensin II. Na/H exchange was measured in rat proximal tubules as the rate of intracellular pH (pHi) recovery in fluorescent units/s. Replacing 5 mmol/L glucose with 5 mmol/L fructose increased the rate of pHi recovery (1.8±0.6 fluorescent units/s; P<0.02; n=8). Staurosporine, a protein kinase C inhibitor, blocked this effect. We studied whether this effect was because of the addition of fructose or removal of glucose. The basal rate of pHi recovery was first tested in the presence of a 0.6-mmol/L glucose and 1, 3, or 5 mmol/L fructose added in a second period. The rate of pHi recovery did not change with 1 mmol/L but it increased with 3 and 5 mmol/L of fructose. Adding 5 mmol/L glucose caused no change. Removal of luminal sodium blocked pHi recovery. With 5.5 mmol/L glucose, angiotensin II (1 pmol/L) did not affect the rate of pHi recovery (change, -1.1±0.5 fluorescent units/s; n=9) but it increased the rate of pHi recovery with 0.6 mmol/L glucose/5 mmol/L fructose (change, 4.0±2.2 fluorescent units/s; P<0.02; n=6). We conclude that fructose stimulates Na/H exchange activity and sensitizes the proximal tubule to angiotensin II. This mechanism is likely dependent on protein kinase C. These results may partially explain the mechanism by which a fructose diet induces hypertension.
Hypertension.Hypertension.2014 Mar;63(3):e68-73. doi: 10.1161/HYPERTENSIONAHA.113.02564. Epub 2013 Dec 30.
The proximal nephron reabsorbs 60% to 70% of the fluid and sodium and most of the filtered bicarbonate via Na/H exchanger 3. Enhanced proximal nephron transport is implicated in hypertension. Our findings show that a fructose-enriched diet causes salt sensitivity. We hypothesized that fructose stimu
PMID 24379189

Filaggrin deficiency leads to impaired lipid profile and altered acidification pathways in a 3D skin construct.

Vávrová K1, Henkes D2, Strüver K3, Sochorová M1, Skolová B1, Witting MY3, Friess W3, Schreml S4, Meier RJ5, Schäfer-Korting M2, Fluhr JW6, Küchler S2.Author information 1Faculty of Pharmacy, Charles University in Prague, Hradec Kralove, Czech Republic.2Institute for Pharmacy, Pharmacology and Toxicology, Freie Universität Berlin, Berlin, Germany.3Department of Pharmacy, Ludwig-Maximilians University Munich, Munich, Germany.4Department of Dermatology, University Medical Center Regensburg, Regensburg, Germany.5Institute of Analytical Chemistry, Chemo- and Biosensors, University of Regensburg, Regensburg, Germany.6Department of Dermatology, Charité University Clinic, Berlin, Germany.AbstractMutations in the filaggrin (FLG) gene are strongly associated with common dermatological disorders such as atopic dermatitis. However, the exact underlying pathomechanism is still ambiguous. Here, we investigated the impact of FLG on skin lipid composition, organization, and skin acidification using a FLG knockdown (FLG-) skin construct. Initially, sodium/hydrogen antiporter (NHE-1) activity was sufficient to maintain the acidic pH (5.5) of the reconstructed skin. At day 7, the FLG degradation products urocanic (UCA) and pyrrolidone-5-carboxylic acid (PCA) were significantly decreased in FLG- constructs, but the skin surface pH was still physiological owing to an upregulation of NHE-1. At day 14, secretory phospholipase A2 (sPLA2) IIA, which converts phospholipids to fatty acids, was significantly more activated in FLG- than in FLG+. Although NHE-1 and sPLA2 were able to compensate the FLG deficiency, maintain the skin surface pH, and ensured ceramide processing (no differences detected), an accumulation of free fatty acids (2-fold increase) led to less ordered intercellular lipid lamellae and higher permeability of the FLG- constructs. The interplay of the UCA/PCA and the sPLA2/NHE-1 acidification pathways of the skin and the impact of FLG insufficiency on skin lipid composition and organization in reconstructed skin are described.
The Journal of investigative dermatology.J Invest Dermatol.2014 Mar;134(3):746-53. doi: 10.1038/jid.2013.402. Epub 2013 Sep 23.
Mutations in the filaggrin (FLG) gene are strongly associated with common dermatological disorders such as atopic dermatitis. However, the exact underlying pathomechanism is still ambiguous. Here, we investigated the impact of FLG on skin lipid composition, organization, and skin acidification using
PMID 24061166

CD44 targets Na(+)/H(+) exchanger 1 to mediate MDA-MB-231 cells' metastasis via the regulation of ERK1/2.

Chang G1, Wang J2, Zhang H2, Zhang Y2, Wang C2, Xu H2, Zhang H2, Lin Y2, Ma L2, Li Q2, Pang T2.Author information 11] State key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China [2] Department of Neurology, Tianjin Medical University General Hospital; Tianjin Neurological Institute; Key Laboratory of Post-trauma Neuro-repair and Regeneration in Central Nervous System, Ministry of Education; Tianjin Key Laboratory of Injuries, Variations and Regeneration of Nervous System, Anshan Road, Tianjin 300052, China.2State key Laboratory of Experimental Hematology, Institute of Hematology and Hospital of Blood Diseases, Chinese Academy of Medical Sciences and Peking Union Medical College, Nanjing Road 288, Tianjin 300020, China.AbstractBACKGROUND: CD44, a transmembrane glycoprotein expressed in a variety of cells and tissues, has been implicated in tumour metastasis. But the molecular mechanisms of CD44-mediated tumour cell metastasis remain to be elucidated.
British journal of cancer.Br J Cancer.2014 Feb 18;110(4):916-27. doi: 10.1038/bjc.2013.809. Epub 2014 Jan 16.
BACKGROUND: CD44, a transmembrane glycoprotein expressed in a variety of cells and tissues, has been implicated in tumour metastasis. But the molecular mechanisms of CD44-mediated tumour cell metastasis remain to be elucidated.METHODS: The downregulation of CD44 was determined by immunofluorescence.
PMID 24434427

Japanese Journal

A shaE Deletion Mutant Showed Lower Na^+ Sensitivity Compared to Other Deletion Mutants in the Bacillus subtilis Sodium/Hydrogen Antiporter (Sha) System

Yoshinaka Toko,Takasu Hirotoshi,Tomizawa Rui [他],KOSONO SAORI,KUDO TOSHIAKI
Journal of bioscience and bioengineering 95(3), 306-309, 2003-03-25
… The sodium/hydrogen antiporter (Sha, identical to multiple resistance and pH adaptation: Mrp) encoded by shaABCDEFG is considered to be the major Na^+ excretion system in Bacillus subtilis. …
NAID 110002665101

A shaE Deletion Mutant Showed Lower Na+ Sensitivity Compared to Other Deletion Mutants in the Bacillus subtilis Sodium/Hydrogen Antiporter (Sha) System

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Journal of Bioscience and Bioengineering 95(3), 306-309, 2003
… The sodium/hydrogen antiporter (Sha, identical to multiple resistance and pH adaptation: Mrp) encoded by shaABCDEFG is considered to be the major Na+ excretion system in Bacillus subtilis. …
NAID 130004056819

The Myocardial Sodium-hydrogen Exchanger (NHE) and Its Role in Mediating Ischemic and Reperfusion Injury

Keio journal of medicine 47(2), 65-72, 1998-06-01
… A major mechanism by which the heart adapts to intracellular acidosis during ischemia and recovers from the acidosis after reperfusion is through the sodium-hydrogen exchanger (NHE). … In addition, NHE-1 expression in the diseased myocardium is increased suggesting that elevated production of the antiporter represents a long-term adaptive process in an attempt by the cardiac cell to regulate intracellular pH which, paradoxically, contributes to cardiac pathology. …
NAID 10020455468