Výsledky vyhledávání - "Ulla G. Friis"

Akademický článek

Plasminogen Deficiency and Amiloride Mitigate Angiotensin II–Induced Hypertension in Type 1 Diabetic Mice Suggesting Effects Through the Epithelial Sodium Channel

Autor: Henrik Andersen, Maria Høj Hansen, Kristian B. Buhl, Mette Stæhr, Ulla G. Friis, Camilla Enggaard, Shanya Supramaniyam, Ida K. Lund, Per Svenningsen, Pernille B. L. Hansen, Boye L. Jensen

Publikováno v: Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease, Vol 9, Iss 23 (2020)

Background Diabetic nephropathy is a common diabetes mellitus complication associated with hypertension, proteinuria, and excretion of urinary plasmin that activates the epithelial sodium channel, ENaC, in vitro. Here we hypothesized that the deletio

Externí odkaz: https://doaj.org/article/89e4a8d381294e9883111bf18a955826

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Sodium retention by uPA‐plasmin‐ENaC in nephrotic syndrome—Authors reply

Autor: Rikke Nielsen, Géraldine Mollet, Ida K. Lund, Henrik Birn, Gitte R. Hinrichs, Boye L. Jensen, Per Svenningsen, Claus Bistrup, Ulla G. Friis, Corinne Antignac, Kathrin Weyer

Publikováno v: Hinrichs, G R, Weyer, K, Friis, U G, Svenningsen, P, Lund, I K, Nielsen, R, Mollet, G, Antignac, C, Bistrup, C, Jensen, B L & Birn, H 2020, ' Sodium retention by uPA-plasmin-ENaC in nephrotic syndrome-Authors reply ', Acta Physiologica
, vol. 228, no. 4, e13432 . https://doi.org/10.1111/apha.13432
Hinrichs, G R, Weyer, K, Friis, U G, Svenningsen, P, Lund, I K, Nielsen, R, Mollet, G, Antignac, C, Bistrup, C, Jensen, B L & Birn, H 2020, ' Sodium retention by uPA-plasmin-ENaC in nephrotic syndrome : Authors reply ', Acta Physiologica

There is a great interest in exploring the mechanisms of oedema in nephrotic syndrome (NS) as evidenced by 2 parallel studies published in Acta Physiologica (1, 2). This has generated an editorial comment (3) which we respond to by this rebuttal. The

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::a33866c5f169d8ef3fe715eb61ac2102
https://doi.org/10.1111/apha.13432

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Plasminogen Deficiency and Amiloride Mitigate Angiotensin II-Induced Hypertension in Type 1 Diabetic Mice Suggesting Effects Through the Epithelial Sodium Channel

Autor: Ida K. Lund, Shanya Supramaniyam, Boye L. Jensen, Camilla Enggaard, Maria H. Hansen, Henrik J. Andersen, Mette Staehr, Per Svenningsen, Ulla G. Friis, Pernille B. Lærkegaard Hansen, Kristian B Buhl

Publikováno v: Andersen, H, Hansen, M H, Buhl, K B, Staehr, M, Friis, U G, Enggaard, C, Supramaniyam, S, Lund, I K, Svenningsen, P, Hansen, P B L & Jensen, B L 2020, ' Plasminogen Deficiency and Amiloride Mitigate Angiotensin II-Induced Hypertension in Type 1 Diabetic Mice Suggesting Effects Through the Epithelial Sodium Channel ', Journal of the American Heart Association, vol. 9, no. 23, 016387, pp. 1-36 . https://doi.org/10.1161/JAHA.120.016387
Journal of the American Heart Association: Cardiovascular and Cerebrovascular Disease
Andersen, H, Hansen, M H, Buhl, K B, Stæhr, M, Friis, U G, Enggaard, C, Supramaniyam, S, Lund, I K, Svenningsen, P, Hansen, P B L & Jensen, B L 2020, ' Plasminogen Deficiency and Amiloride Mitigate Angiotensin II-Induced Hypertension in Type 1 Diabetic Mice Suggesting Effects Through the Epithelial Sodium Channel ', Journal of the American Heart Association, vol. 9, no. 23, e016387 . https://doi.org/10.1161/JAHA.120.016387

BackgroundDiabetic nephropathy is a common diabetes mellitus complication associated with hypertension, proteinuria, and excretion of urinary plasmin that activates the epithelial sodium channel, ENaC, in vitro. Here we hypothesized that the deletion

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8ec5e6af86e7d6210a98217a6c0a40d4
https://curis.ku.dk/portal/da/publications/plasminogen-deficiency-and-amiloride-mitigate-angiotensin-iiinduced-hypertension-in-type-1-diabetic-mice-suggesting-effects-through-the-epithelial-sodium-channel(19a2798d-5153-41b9-bfa6-5dc8a2fdb58d).html

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Urokinase‐type plasminogen activator contributes to amiloride‐sensitive sodium retention in nephrotic range glomerular proteinuria in mice

Autor: Gitte R. Hinrichs, Boye L. Jensen, Rikke Nielsen, Géraldine Mollet, Henrik Birn, Ulla G. Friis, Corinne Antignac, Kathrin Weyer, Per Svenningsen, Ida K. Lund, Claus Bistrup

Publikováno v: Hinrichs, G R, Weyer, K, Friis, U G, Svenningsen, P, Lund, I K, Nielsen, R, Mollet, G, Antignac, C, Bistrup, C, Jensen, B L & Birn, H 2019, ' Urokinase-type plasminogen activator contributes to amiloride-sensitive sodium retention in nephrotic range glomerular proteinuria in mice ', Acta Physiologica, vol. 227, no. 4, e13362 . https://doi.org/10.1111/apha.13362
Hinrichs, G R, Weyer, K, Friis, U G, Svenningsen, P, Lund, I K, Nielsen, R, Mollet, G, Antignac, C, Bistrup, C, Jensen, B L & Birn, H 2019, ' Urokinase-type plasminogen activator contributes to amiloride-sensitive sodium retention in nephrotic range glomerular proteinuria in mice ', Acta Physiologica (Online), vol. 227, no. 4, e13362 . https://doi.org/10.1111/apha.13362

AIM: Activation of sodium reabsorption by urinary proteases has been implicated in sodium retention associated with nephrotic syndrome. The study was designed to test the hypothesis that nephrotic proteinuria in mice after conditional deletion of pod

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1505f3e8eb4b67f1cf8a563835045474
https://doi.org/10.1111/apha.13362

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Albuminuria in kidney transplant recipients is associated with increased urinary serine proteases and activation of the epithelial sodium channel

Autor: Rikke Zachar, Jannie Solmunde Michelsen, Per Svenningsen, Gitte R. Hinrichs, Boye L. Jensen, Henrik Birn, Claus Bistrup, Ulla G. Friis

Publikováno v: Hinrichs, G R, Michelsen, J S, Zachar, R, Friis, U G, Svenningsen, P, Birn, H, Bistrup, C & Jensen, B L 2018, ' Albuminuria in kidney transplant recipients is associated with increased urinary serine proteases and activation of the epithelial sodium channel ', American Journal of Physiology: Renal Physiology, vol. 315, no. 1, pp. F151-F160 . https://doi.org/10.1152/ajprenal.00545.2017

Albuminuria predicts adverse renal outcome in kidney transplant recipients. The present study addressed the hypothesis that albuminuria is associated with increased urine serine proteases with the ability to activate the epithelial sodium channel (EN

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1bb353161bff56657574b3b180a3b300
https://pubmed.ncbi.nlm.nih.gov/29363322

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Diabetic nephropathy is associated with increased urine excretion of proteases plasmin, prostasin and urokinase and activation of amiloride-sensitive current in collecting duct cells

Autor: Per Svenningsen, Jan Erik Henriksen, Boye L. Jensen, Henrik Andersen, Ulla G. Friis, Pernille B. Lærkegaard Hansen

Publikováno v: Andersen, H, Friis, U G, Hansen, P B L, Svenningsen, P, Henriksen, J E & Jensen, B L 2015, ' Diabetic nephropathy is associated with increased urine excretion of proteases plasmin, prostasin and urokinase and activation of amiloride-sensitive current in collecting duct cells ', Nephrology, Dialysis, Transplantation, vol. 30, no. 5, pp. 781-789 . https://doi.org/10.1093/ndt/gfu402

BACKGROUND: Diabetic nephropathy (DN) is associated with hypertension, expanded extracellular volume and impaired renal Na(+) excretion. It was hypothesized that aberrant glomerular filtration of serine proteases in DN causes proteolytic activation o

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::eb9c5e6787cf29e21a98617a1ab4226d
https://doi.org/10.1093/ndt/gfu402

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Plasmin in urine from patients with type 2 diabetes and treatment-resistant hypertension activates ENaC in vitro

Autor: Kristian B Buhl, Boye L. Jensen, Claus Bistrup, Ib Abildgaard Jacobsen, Christina Stolzenburg Oxlund, Ulla G. Friis, Per Svenningsen

Publikováno v: Buhl, K B, Stolzenburg Oxlund, C, Friis, U G, Svenningsen, P, Bistrup, C, Jacobsen, I A & Jensen, B L 2014, ' Plasmin in urine from patients with type 2 diabetes and treatment-resistant hypertension activates ENaC in vitro ', Journal of Hypertension, vol. 32, no. 8, pp. 1672–1677 . https://doi.org/10.1097/HJH.0000000000000216

Aberrant filtration of plasminogen from plasma and subsequent activation to plasmin in the urinary space may activate proteolytically the epithelial sodium channel, ENaC. In conditions with chronic albuminuria, this may cause hypertension. It was hyp

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::dbbc55e5b21be0e9170183c830fb52d1
https://doi.org/10.1097/hjh.0000000000000216

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Remission of nephrotic syndrome diminishes urinary plasmin content and abolishes activation of ENaC

Autor: René Frydensbjerg Andersen, Boye L. Jensen, Ulla G. Friis, Kristian B Buhl, Bente Jespersen, Per Svenningsen, Søren Rittig

Publikováno v: Andersen, R F, Buhl, K B, Jensen, B L, Svenningsen, P, Friis, U G, Jespersen, B & Rittig, S 2013, ' Remission of nephrotic syndrome diminishes urinary plasmin content and abolishes activation of ENaC ', Pediatric nephrology (Berlin, Germany), vol. 28, no. 8, pp. 1227-34 . https://doi.org/10.1007/s00467-013-2439-2
Andersen, M R, Buhl, K B, Jensen, B L, Svenningsen, P, Friis, U G, Jespersen, B & Rittig, S 2013, ' Remission of nephrotic syndrome diminishes urinary plasmin content and abolishes activation of ENaC ', Pediatric Nephrology, vol. 28, no. 8, pp. 1227-1234 . https://doi.org/10.1007/s00467-013-2439-2

Background: Urinary plasmin activates the epithelial Na + channel (ENaC) in vitro and may possibly be a mechanism of sodium retention in nephrotic syndrome (NS). This study used a paired design to test the hypothesis that remission of NS is associate

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d496afd4f8636a6596b4525b656197e2
https://doi.org/10.1007/s00467-013-2439-2

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Regulation of renin secretion by renal juxtaglomerular cells

Autor: Jane Stubbe, Ole Skøtt, Pernille B. Lærkegaard Hansen, Per Svenningsen, Ulla G. Friis, Kirsten Madsen, Peter Bie, Boye L. Jensen

Publikováno v: Friis, U G, Madsen, K, Stubbe, J, Hansen, P B L, Svenningsen, P, Bie, P, Skøtt, O & Jensen, B L 2013, ' Regulation of renin secretion by renal juxtaglomerular cells ', Pflügers Archiv-European Journal of Physiology, vol. 465, no. 1, pp. 25-37 . https://doi.org/10.1007/s00424-012-1126-7

A major rate-limiting step in the renin-angiotensin-aldosterone system is the release of active renin from endocrine cells (juxtaglomerular (JG) cells) in the media layer of the afferent glomerular arterioles. The number and distribution of JG cells

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::b127043728bde2c29aef035d4fd3a4ac
https://doi.org/10.1007/s00424-012-1126-7

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Intracellular signalling pathways in the vasoconstrictor response of mouse afferent arterioles to adenosine

Autor: Torben Rene Uhrenholt, Josie P. Briggs, Pernille B. Lærkegaard Hansen, Ulla G. Friis, Jurgen Schnermann

Publikováno v: Hansen, P B L, Friis, U G, Uhrenholt, T R, Briggs, J & Schnermann, J 2007, ' Intracellular signalling pathways in the vasoconstrictor response of mouse afferent arterioles to adenosine ', Acta Physiologica (Print Edition), vol. 191, no. 2, pp. 89-97 . https://doi.org/10.1111/j.1748-1716.2007.01724.x

Udgivelsesdato: 2007-Oct AIMS: Adenosine causes vasoconstriction of afferent arterioles of the mouse kidney through activation of adenosine A(1) receptors and Gi-mediated stimulation of phospholipase C. In the present study, we further explored the s

Externí odkaz: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::ec7c8a8483c67226a6ffc1e6e985e1fa
https://doi.org/10.1111/j.1748-1716.2007.01724.x

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