Zobrazeno 1 - 10
of 12
pro vyhledávání: '"Kristian B Buhl"'
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
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
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
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
Autor:
Rikke Ydegaard, Boye L. Jensen, Maria Ravn Nielsen, Mie R. Hansen, Per Svenningsen, Rikke Zachar, Jan Stener Jørgensen, Britta Frederiksen-Møller, Kristian B Buhl
Publikováno v:
Nielsen, M R, Frederiksen-Møller, B, Langkilde, R Z, Jørgensen, J S, Rytz, M, Ydegaard, R, Svenningsen, P, Buhl, K B & Jensen, B L 2017, ' Urine exosomes from healthy and hypertensive pregnancies display elevated level of-α-subunit and cleaved-α-and γ-subunits of the epithelial sodium channel--ENaC ', Pflügers Archiv-European Journal of Physiology, vol. 469, no. 9, pp. 1107–1119 . https://doi.org/10.1007/s00424-017-1977-z
Preeclampsia is characterized by hypertension, proteinuria, suppression of plasma renin-angiotensin-aldosterone, and impaired urine sodium excretion. Aberrantly filtered plasmin in urine may activate proteolytically the γ-subunit of the epithelial s
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::64d88cafe975135e426f358ed2c62ed1
https://doi.org/10.1007/s00424-017-1977-z
https://doi.org/10.1007/s00424-017-1977-z
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
https://doi.org/10.1097/hjh.0000000000000216
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
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
https://doi.org/10.1007/s00467-013-2439-2
Autor:
Per Svenningsen, René Frydensbjerg Andersen, Kristian B Buhl, Gitte Rye Hinrichs, Claus Bistrup, Flemming Nielsen, Boye L. Jensen, Mette Staehr
Publikováno v:
Staehr, M, Buhl, K B, Andersen, R F, Svenningsen, P, Nielsen, F, Hinrichs, G R, Bistrup, C & Jensen, B L 2015, ' Aberrant glomerular filtration of urokinase-type plasminogen activator in nephrotic syndrome leads to amiloride-sensitive plasminogen activation in urine ', American Journal of Physiology: Renal Physiology, vol. 309, no. 3, pp. F235-41 . https://doi.org/10.1152/ajprenal.00138.2015
Stæhr, M, Buhl, K B, Andersen, R F, Svenningsen, P, Nielsen, F, Hinrichs, G R, Bistrup, C & Jensen, B L 2015, ' Aberrant glomerular filtration of urokinase-type plasminogen activator in nephrotic syndrome leads to amiloride-sensitive plasminogen activation in urine ', American Journal of Physiology: Renal Physiology, vol. 309, no. 3, pp. F235-F241 . https://doi.org/10.1152/ajprenal.00138.2015
Stæhr, M, Buhl, K B, Andersen, R F, Svenningsen, P, Nielsen, F, Hinrichs, G R, Bistrup, C & Jensen, B L 2015, ' Aberrant glomerular filtration of urokinase-type plasminogen activator in nephrotic syndrome leads to amiloride-sensitive plasminogen activation in urine ', American Journal of Physiology: Renal Physiology, vol. 309, no. 3, pp. F235-F241 . https://doi.org/10.1152/ajprenal.00138.2015
In nephrotic syndrome, aberrant glomerular filtration of plasminogen and conversion to active plasmin in preurine are thought to activate proteolytically epithelial sodium channel (ENaC) and contribute to sodium retention and edema. The ENaC blocker
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1735cbd9aefee181fc1504624048d15c
https://pubmed.ncbi.nlm.nih.gov/26084931
https://pubmed.ncbi.nlm.nih.gov/26084931
Autor:
Ib Abildgaard Jacobsen, Mie R. Hansen, Jeppe Gram, Karoline Schousboe, Boye L. Jensen, Kristian B Buhl, Christina Stolzenburg Oxlund, Lise Tarnow, Jan Erik Henriksen
Publikováno v:
Stolzenburg Oxlund, C, Buhl, K B, Jacobsen, I A, Hansen, M R, Gram, J, Henriksen, J E, Schousboe, K, Tarnow, L & Jensen, B L 2014, ' Amiloride lowers blood pressure and attenuates urine plasminogen activation in patients with treatment-resistant hypertension ', American Society of Hypertension. Journal, vol. 8, no. 12, pp. 872-881 . https://doi.org/10.1016/j.jash.2014.09.019
In conditions with albuminuria, plasminogen is aberrantly filtered across the glomerular barrier and activated along the tubular system to plasmin. In the collecting duct, plasmin activates epithelial sodium channels (ENaC) proteolytically. Hyperacti
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::2db9b4d9e05bcc953b6750e5bab13ef3
https://pubmed.ncbi.nlm.nih.gov/25492830
https://pubmed.ncbi.nlm.nih.gov/25492830
Autor:
Ib Abildgaard Jacobsen, Boye L. Jensen, Kristian B Buhl, Per Svenningsen, Claus Bistrup, Ulla G. Friis, Christina Stolzenburg Oxlund
Publikováno v:
Friis, U G, Buhl, K B, Svenningsen, P, Bistrup, C, Stolzenburg Oxlund, C, Jacobsen, I A & Jensen, B L 2013, ' Type 2 diabetic patients with treatment-resistant hypertension display urine plasmin excretion that correlate with blood pressure and activate ENaC current ' .
University of Southern Denmark
University of Southern Denmark
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::32984b62fd84186b56702579c2f8c59c
https://portal.findresearcher.sdu.dk/da/publications/b9a50583-81b9-44fc-9cd1-823be753fc60
https://portal.findresearcher.sdu.dk/da/publications/b9a50583-81b9-44fc-9cd1-823be753fc60
Autor:
Ole Skøtt, Boye L. Jensen, René Frydensbjerg Andersen, Per Svenningsen, Ulla G. Friis, J. B. Versland, Rikke Zachar, Jan Stener Jørgensen, B. Møller Frederiksen, Kristian B Buhl, Claus Bistrup, Henrik Andersen
Publikováno v:
Svenningsen, P, Friis, U G, Versland, J B, Buhl, K B, Frederiksen-Møller, B, Andersen, H, Zachar, R M, Bistrup, C, Skøtt, O, Jørgensen, J S, Andersen, R F & Jensen, B L 2013, ' Mechanisms of renal NaCl retention in proteinuric disease ', Acta Physiologica
, vol. 207, no. 3, pp. 536-545 . https://doi.org/10.1111/apha.12047
, vol. 207, no. 3, pp. 536-545 . https://doi.org/10.1111/apha.12047
In diseases with proteinuria, for example nephrotic syndrome and pre-eclampsia, there often are suppression of plasma renin-angiotensin-aldosterone system components, expansion of extracellular volume and avid renal sodium retention. Mechanisms of so
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::1e426199f249914df7bd0a7082c67ce0
https://pubmed.ncbi.nlm.nih.gov/23216619
https://pubmed.ncbi.nlm.nih.gov/23216619
Publikováno v:
The FASEB Journal. 26
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::f4a5964821bc23535b88614860e26888
https://doi.org/10.1096/fasebj.26.1_supplement.868.13
https://doi.org/10.1096/fasebj.26.1_supplement.868.13