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  1. Article: Pharmacology of Compounds Targeting Cation-Chloride Cotransporter Physiology.

    Delpire, Eric / Terker, Andrew S / Gagnon, Kenneth B

    Handbook of experimental pharmacology

    2023  Volume 283, Page(s) 249–284

    Abstract: Transporters of the solute carrier family 12 (SLC12) carry inorganic cations such as ... ...

    Abstract Transporters of the solute carrier family 12 (SLC12) carry inorganic cations such as Na
    MeSH term(s) Humans ; Sodium-Potassium-Chloride Symporters/metabolism ; Chlorides/metabolism ; Cryoelectron Microscopy ; Solute Carrier Family 12, Member 3 ; Cations/metabolism
    Chemical Substances Sodium-Potassium-Chloride Symporters ; Chlorides ; Solute Carrier Family 12, Member 3 ; Cations
    Language English
    Publishing date 2023-08-11
    Publishing country Germany
    Document type Journal Article
    ISSN 0171-2004
    ISSN 0171-2004
    DOI 10.1007/164_2023_692
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    Sign. bis Bd. 125 (1997): 1982 A 2146: Show issues
     danach: Sign. bei den Einzelbänden: Show issues

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  2. Article ; Online: Untangling the fibers of sarcopenia: activin A in chronic kidney disease-associated muscle wasting.

    Terker, Andrew S / Ikizler, T Alp

    Kidney international

    2021  Volume 101, Issue 2, Page(s) 211–213

    MeSH term(s) Activins ; Humans ; Muscles ; Muscular Atrophy ; Renal Insufficiency, Chronic/complications ; Sarcopenia/etiology
    Chemical Substances activin A ; Activins (104625-48-1)
    Language English
    Publishing date 2021-10-27
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 120573-0
    ISSN 1523-1755 ; 0085-2538
    ISSN (online) 1523-1755
    ISSN 0085-2538
    DOI 10.1016/j.kint.2021.08.034
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    Zs.A 797: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: The Highs and Lows of Potassium Intake in CKD-Does One Size Fit All?

    Terker, Andrew S / Saritas, Turgay / McDonough, Alicia A

    Journal of the American Society of Nephrology : JASN

    2022  Volume 33, Issue 9, Page(s) 1638–1640

    MeSH term(s) Humans ; Renal Insufficiency, Chronic ; Potassium ; Potassium, Dietary
    Chemical Substances Potassium (RWP5GA015D) ; Potassium, Dietary
    Language English
    Publishing date 2022-07-19
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Comment
    ZDB-ID 1085942-1
    ISSN 1533-3450 ; 1046-6673
    ISSN (online) 1533-3450
    ISSN 1046-6673
    DOI 10.1681/ASN.2022070743
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    Zs.A 3344: Show issues Location:
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    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Staying Connected: Transcriptomics in the Search for Novel Diabetic Kidney Disease Treatments.

    Terker, Andrew S / Zhang, Ming-Zhi / Harris, Raymond C

    Diabetes

    2021  Volume 70, Issue 2, Page(s) 326–327

    MeSH term(s) Diabetes Mellitus ; Diabetic Nephropathies/genetics ; Humans ; Pharmaceutical Preparations ; Pteridines ; Transcriptome
    Chemical Substances BI 2536 ; Pharmaceutical Preparations ; Pteridines
    Language English
    Publishing date 2021-01-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Comment
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/dbi20-0042
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    Uh III Zs.175: Show issues Location:
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  5. Article ; Online: High sodium intake does not worsen low potassium-induced kidney damage.

    Zhang, Yahua / Arroyo, Juan Pablo / Bock, Fabian / Zhang, Ming-Zhi / Harris, Raymond C / Terker, Andrew S

    Physiological reports

    2023  Volume 11, Issue 8, Page(s) e15671

    Abstract: High sodium and low potassium intake have both been linked to poor cardiovascular health outcomes and increased mortality rates. A combination of the two is thought to be particularly detrimental. While mechanisms are multiple, the kidney is an important ...

    Abstract High sodium and low potassium intake have both been linked to poor cardiovascular health outcomes and increased mortality rates. A combination of the two is thought to be particularly detrimental. While mechanisms are multiple, the kidney is an important target of harmful effects and low potassium influences on both proximal and distal nephron segments are especially potent. We recently reported that a combined high sodium/low potassium diet causes kidney injury and that low potassium in isolation can have similar effects. However, how sodium intake alters this process is not well-understood. Here we tested the hypothesis that a high sodium intake amplifies effects of low dietary potassium on kidney injury. We observed adding high sodium to low potassium caused an expected increase in blood pressure, but did not worsen markers of kidney injury, inflammation, and fibrosis. It also did not increase abundance or phosphorylation of the sodium chloride cotransporter or its regulatory kinases, SPAK and OxSR1, known renal targets of low potassium. Findings support the claim that dietary potassium deficiency, and not high sodium, is a dominant factor affecting kidney injury in animal models of high sodium/low potassium intake. This suggests further investigation is required to identify optimal ranges of sodium and potassium intake in both healthy populations and in those with kidney disease.
    MeSH term(s) Animals ; Kidney ; Sodium ; Kidney Diseases ; Potassium ; Sodium, Dietary/adverse effects
    Chemical Substances Sodium (9NEZ333N27) ; Potassium (RWP5GA015D) ; Sodium, Dietary
    Language English
    Publishing date 2023-04-20
    Publishing country United States
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2724325-4
    ISSN 2051-817X ; 2051-817X
    ISSN (online) 2051-817X
    ISSN 2051-817X
    DOI 10.14814/phy2.15671
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Bicarbonate is the primary inducer of KCC3a expression in renal cortical B-type intercalated cells.

    Ferdaus, Mohammed Z / Terker, Andrew S / Koumangoye, Rainelli / Wall, Susan M / Delpire, Eric

    American journal of physiology. Cell physiology

    2023  Volume 324, Issue 5, Page(s) C1171–C1178

    Abstract: A primary function of intercalated cells in the distal tubule of the kidney is to maintain pH homeostasis. For example, type B intercalated cells secrete bicarbonate largely through the action of the apical ... ...

    Abstract A primary function of intercalated cells in the distal tubule of the kidney is to maintain pH homeostasis. For example, type B intercalated cells secrete bicarbonate largely through the action of the apical Cl
    MeSH term(s) Animals ; Mice ; Bicarbonates/metabolism ; Aldosterone/pharmacology ; Aldosterone/metabolism ; Angiotensin II/pharmacology ; Angiotensin II/metabolism ; Kidney/metabolism ; Sulfate Transporters/genetics ; Sulfate Transporters/metabolism ; Alkalosis/metabolism ; Anion Transport Proteins/genetics
    Chemical Substances Bicarbonates ; Aldosterone (4964P6T9RB) ; Angiotensin II (11128-99-7) ; Sulfate Transporters ; Anion Transport Proteins
    Language English
    Publishing date 2023-04-10
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 392098-7
    ISSN 1522-1563 ; 0363-6143
    ISSN (online) 1522-1563
    ISSN 0363-6143
    DOI 10.1152/ajpcell.00094.2023
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    Uc I Zs.89: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  7. Article ; Online: Renal mineralocorticoid receptor and electrolyte homeostasis.

    Terker, Andrew S / Ellison, David H

    American journal of physiology. Regulatory, integrative and comparative physiology

    2015  Volume 309, Issue 9, Page(s) R1068–70

    Abstract: The renal mineralocorticoid receptor (MR) is a steroid hormone receptor essential for maintaining electrolyte homeostasis. Its role in mediating effects of aldosterone was likely vital in enabling the evolution of terrestrial life. Dysregulated ... ...

    Abstract The renal mineralocorticoid receptor (MR) is a steroid hormone receptor essential for maintaining electrolyte homeostasis. Its role in mediating effects of aldosterone was likely vital in enabling the evolution of terrestrial life. Dysregulated aldosterone-MR signaling has been identified as the cause of multiple clinical diseases, suggesting the physiological importance of the MR. While the physiology of this pathway has been studied for over 60 years, only more recently have genetic mouse models been available to dissect its function in vivo. This review will focus on recent advances in our knowledge of MR function with an emphasis on these models.
    MeSH term(s) Aldosterone/metabolism ; Animals ; Blood Pressure/physiology ; Humans ; Ion Channel Gating/physiology ; Kidney/physiology ; Models, Biological ; Potassium/metabolism ; Potassium Channels/metabolism ; Receptors, Mineralocorticoid ; Water-Electrolyte Balance
    Chemical Substances Potassium Channels ; Receptors, Mineralocorticoid ; Aldosterone (4964P6T9RB) ; Potassium (RWP5GA015D)
    Language English
    Publishing date 2015-07-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00135.2015
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    Uc I Zs.89: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
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  8. Article: Why Your Mother Was Right: How Potassium Intake Reduces Blood Pressure.

    Ellison, David H / Terker, Andrew S

    Transactions of the American Clinical and Climatological Association

    2015  Volume 126, Page(s) 46–55

    Abstract: Low potassium intake, common in western diets, increases blood pressure and enhances salt-sensitivity. Most humans in "Westernized" countries also consume excess salt. In studies using mice, we found that a high-salt, low-potassium diet activates the ... ...

    Abstract Low potassium intake, common in western diets, increases blood pressure and enhances salt-sensitivity. Most humans in "Westernized" countries also consume excess salt. In studies using mice, we found that a high-salt, low-potassium diet activates the thiazide-sensitive Na-Cl cotransporter in the kidney. This effect led to sodium retention and increased blood pressure, and was dependent on plasma potassium. We postulated that this effect was mediated by changes in intracellular chloride caused by changes in membrane voltage. We developed a model in cultured cells permitting us to confirm this hypothesis. We then confirmed, using urinary exosomes, that dietary changes in normal humans, affect the thiazide-sensitive Na-Cl cotransporter in the same way. These data show that dietary potassium deficiency increases blood pressure largely by stimulating salt reabsorption along the distal nephron. They suggest that global efforts should focus on increasing potassium intake, which will attenuate the effects of high-salt diets.
    MeSH term(s) Animals ; Blood Pressure ; HEK293 Cells ; Humans ; Hypertension/diet therapy ; Hypertension/metabolism ; Hypertension/physiopathology ; Kidney/metabolism ; Kidney/physiopathology ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Phosphorylation ; Potassium Deficiency/diet therapy ; Potassium Deficiency/metabolism ; Potassium Deficiency/physiopathology ; Potassium, Dietary/administration & dosage ; Potassium, Dietary/metabolism ; Solute Carrier Family 12, Member 3/genetics ; Solute Carrier Family 12, Member 3/metabolism ; Time Factors ; Transfection ; Treatment Outcome ; Water-Electrolyte Balance
    Chemical Substances Potassium, Dietary ; SLC12A3 protein, human ; Slc12a3 protein, mouse ; Solute Carrier Family 12, Member 3
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article ; Randomized Controlled Trial ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 603823-2
    ISSN 0065-7778
    ISSN 0065-7778
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 4: Show issues Location:
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  9. Article ; Online: Rac1 promotes kidney collecting duct repair by mechanically coupling cell morphology to mitotic entry.

    Bock, Fabian / Dong, Xinyu / Li, Shensen / Viquez, Olga M / Sha, Eric / Tantengco, Matthew / Hennen, Elizabeth M / Plosa, Erin / Ramezani, Alireza / Brown, Kyle L / Whang, Young Mi / Terker, Andrew S / Arroyo, Juan Pablo / Harrison, David G / Fogo, Agnes / Brakebusch, Cord H / Pozzi, Ambra / Zent, Roy

    Science advances

    2024  Volume 10, Issue 6, Page(s) eadi7840

    Abstract: Prolonged obstruction of the ureter, which leads to injury of the kidney collecting ducts, results in permanent structural damage, while early reversal allows for repair. Cell structure is defined by the actin cytoskeleton, which is dynamically organized ...

    Abstract Prolonged obstruction of the ureter, which leads to injury of the kidney collecting ducts, results in permanent structural damage, while early reversal allows for repair. Cell structure is defined by the actin cytoskeleton, which is dynamically organized by small Rho guanosine triphosphatases (GTPases). In this study, we identified the Rho GTPase, Rac1, as a driver of postobstructive kidney collecting duct repair. After the relief of ureteric obstruction, Rac1 promoted actin cytoskeletal reconstitution, which was required to maintain normal mitotic morphology allowing for successful cell division. Mechanistically, Rac1 restricted excessive actomyosin activity that stabilized the negative mitotic entry kinase Wee1. This mechanism ensured mechanical G
    MeSH term(s) Kidney Tubules, Collecting/metabolism ; rac1 GTP-Binding Protein/metabolism ; Cytoskeleton/metabolism ; Actins/metabolism ; Actin Cytoskeleton/metabolism
    Chemical Substances rac1 GTP-Binding Protein (EC 3.6.5.2) ; Actins
    Language English
    Publishing date 2024-02-07
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.adi7840
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  10. Article ; Online: Randomized Trial on the Effect of Oral Potassium Chloride Supplementation on the Thiazide-Sensitive Sodium Chloride Cotransporter in Healthy Adults.

    Wu, Aihua / Wolley, Martin J / Mayr, Hannah L / Cheng, Lei / Cowley, Diane / Li, Bo / Campbell, Katrina L / Terker, Andrew S / Ellison, David H / Welling, Paul A / Fenton, Robert A / Stowasser, Michael

    Kidney international reports

    2023  Volume 8, Issue 6, Page(s) 1201–1212

    Abstract: Introduction: The putative "renal-K switch" mechanism links dietary potassium intake with sodium retention and involves activation of the sodium chloride (NaCl) cotransporter (NCC) in the distal convoluted tubule in response to low potassium intake, and ...

    Abstract Introduction: The putative "renal-K switch" mechanism links dietary potassium intake with sodium retention and involves activation of the sodium chloride (NaCl) cotransporter (NCC) in the distal convoluted tubule in response to low potassium intake, and suppression in response to high potassium intake. This study examined NCC abundance and phosphorylation (phosphorylated NCC [pNCC]) in urinary extracellular vesicles (uEVs) isolated from healthy adults on a high sodium diet to determine tubular responses to alteration in potassium chloride (KCl) intake.
    Methods: Healthy adults maintained on a high sodium (∼4.5 g [200 mmol]/d) low potassium (∼2.3 g [60 mmol]/d) diet underwent a 5-day run-in period followed by a crossover study, with 5-day supplementary KCl (active phase, Span-K 3 tablets (potassium 24 mmol) thrice daily) or 5-day placebo administrated in random order and separated by 2-day washout. Ambulatory blood pressure (BP) and biochemistries were assessed, and uEVs were analyzed by western blotting.
    Results: Among the 18 participants who met analysis criteria, supplementary KCl administration (vs. placebo) was associated with markedly higher levels of plasma potassium and 24-hour urine excretion of potassium, chloride, and aldosterone. KCl supplementation was associated with lower uEV levels of NCC (median fold change
    Conclusions: The lower NCC and pNCC in uEVs in response to oral KCl supplementation provide evidence to support the hypothesis of a functional "renal-K switch" in healthy human subjects.
    Language English
    Publishing date 2023-03-27
    Publishing country United States
    Document type Journal Article
    ISSN 2468-0249
    ISSN (online) 2468-0249
    DOI 10.1016/j.ekir.2023.03.011
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