Zobrazeno 1 - 8
of 8
pro vyhledávání: '"Niklas, Ayasse"'
Autor:
Babak Yazdani, Marcus E. Kleber, Graciela E. Delgado, Gökhan Yücel, Aruscha Asgari, Andreas L.H. Gerken, Clara Daschner, Niklas Ayasse, Winfried März, Christoph Wanner, Bernhard K. Krämer
Publikováno v:
Kidney & Blood Pressure Research, Pp 1-1 (2023)
Introduction: Systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) are risk factors for cardiovascular mortality (CVM). Pulse pressure (PP) is an easily available parameter of vascular stiffness, but its imp
Externí odkaz:
https://doaj.org/article/c9abfa1668eb4bf7be934703f0137bd9
Autor:
Jesper Frank Andersen, Charles S. Wingo, Jens Leipziger, Niklas Ayasse, I. Jeanette Lynch, Natalya U. Fedosova, Samuel L Svendsen, Mads V. Sorensen, Peder Berg
Publikováno v:
Ayasse, N, Berg, P, Andersen, J F, Svendsen, S L S C, Sørensen, M V, Fedosova, N, Wingo, C, Lynch, I J & Leipziger, J G 2021, ' Benzamil-mediated urine alkalization is caused by the inhibition of H +, K + ATPases ', American Journal of Physiology: Renal Physiology, vol. 320, no. 4, pp. F596-F607 . https://doi.org/10.1152/ajprenal.00444.2020
Epithelial Na+ channel (ENaC) blockers elicit acute and substantial increases of urinary pH. The underlying mechanism remains to be understood. Here, we evaluated if benzamil-induced urine alkalization is mediated by an acute reduction in H+ secretio
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3bb42c5990e38c42a7751b24b66b2eba
https://doi.org/10.1152/ajprenal.00444.2020
https://doi.org/10.1152/ajprenal.00444.2020
Autor:
Niklas, Ayasse, Peder, Berg, Jesper Frank, Andersen, Samuel Levi, Svendsen, Mads V, Sørensen, Natalya U, Fedosova, I Jeanette, Lynch, Charles S, Wingo, Jens, Leipziger
Publikováno v:
American journal of physiology. Renal physiology. 320(4)
Epithelial Na
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::884211b6c22abe78f53da38e06a57856
https://pubmed.ncbi.nlm.nih.gov/33554781
https://pubmed.ncbi.nlm.nih.gov/33554781
Publikováno v:
Ayasse, N, Berg, P, Leipziger, J G & Sørensen, M V 2021, ' ENaC expression correlates with the acute furosemide-induced K + excretion ', Physiological Reports, vol. 9, no. 1 . https://doi.org/10.14814/phy2.14668
Background: In the aldosterone-sensitive distal nephron (ASDN), epithelial sodiumchannel (ENaC)-mediated Na+ absorption drives K+ excretion. K+ excretion dependson the delivery of Na+ to the ASDN and molecularly activated ENaC. Furosemideis known as
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::62d59deb595aabce52e03c231c1017a5
https://pure.au.dk/ws/files/207147678/final_paper.pdf
https://pure.au.dk/ws/files/207147678/final_paper.pdf
Publikováno v:
Physiological Reports
Background In the aldosterone‐sensitive distal nephron (ASDN), epithelial sodium channel (ENaC)‐mediated Na+ absorption drives K+ excretion. K+ excretion depends on the delivery of Na+ to the ASDN and molecularly activated ENaC. Furosemide is kno
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::c1d15c4d81dae114bc9e94c05244c385
https://pubmed.ncbi.nlm.nih.gov/33410279
https://pubmed.ncbi.nlm.nih.gov/33410279
Autor:
David A. Pearce, Peng Wu, Iben Skov Jensen, Wen-Hui Wang, Bidisha Saha, Catherine E. Gleason, Samuel L Svendsen, Mads V. Sorensen, Niklas Ayasse
Publikováno v:
Sørensen, M V, Saha, B, Jensen, I S, Wu, P, Ayasse, N, Gleason, C E, Svendsen, S L, Wang, W H & Pearce, D 2019, ' Potassium acts through mTOR to regulate its own secretion ', JCI Insight, vol. 4, no. 11, e126910 . https://doi.org/10.1172/jci.insight.126910
JCI insight, vol 5, iss 11
JCI insight, vol 5, iss 11
Potassium (K+) secretion by kidney tubule cells is central to electrolyte homeostasis in mammals. In the K+-secreting principal cells of the distal nephron, electrogenic Na+ transport by the epithelial sodium channel (ENaC) generates the electrical d
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::578ad7db2ed3256f46d52d7e4fdd626b
https://pubmed.ncbi.nlm.nih.gov/31013253
https://pubmed.ncbi.nlm.nih.gov/31013253
Autor:
Nina Himmerkus, Alexander Paliege, Carolin Knappe, Katsumasa Kawahara, Sebastian Bachmann, Alina Smorodchenko, Jens Leipziger, Markus Bleich, Julian Isermann, Julia Shpak, Niklas Ayasse, Jan Schmoranzer, Kerim Mutig, Niclas Gimber, Michael Fähling, Taka-aki Koshimizu, Torsten Giesecke
Publikováno v:
Giesecke, T, Himmerkus, N, Leipziger, J, Bleich, M, Koshimizu, T A, Fähling, M, Smorodchenko, A, Shpak, J, Knappe, C, Isermann, J, Ayasse, N, Kawahara, K, Schmoranzer, J, Gimber, N, Paliege, A, Bachmann, S & Mutig, K 2019, ' Vasopressin Increases Urinary Acidification via V1a Receptors in Collecting Duct Intercalated Cells ', Journal of the American Society of Nephrology : JASN, vol. 30, no. 6, pp. 946-961 . https://doi.org/10.1681/ASN.2018080816
J Am Soc Nephrol
J Am Soc Nephrol
Background Antagonists of the V1a vasopressin receptor (V1aR) are emerging as a strategy for slowing progression of CKD. Physiologically, V1aR signaling has been linked with acid-base homeostasis, but more detailed information is needed about renal V
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::92738fb6dd317de6f0e3071e288c268e
https://pure.au.dk/portal/da/publications/vasopressin-increases-urinary-acidification-via-v1a-receptors-in-collecting-duct-intercalated-cells(06767e52-e15b-4f6b-bbf0-5d72327d4b9e).html
https://pure.au.dk/portal/da/publications/vasopressin-increases-urinary-acidification-via-v1a-receptors-in-collecting-duct-intercalated-cells(06767e52-e15b-4f6b-bbf0-5d72327d4b9e).html
Publikováno v:
Ayasse, N, de Bruijn, P I A, Berg, P, Sørensen, M V & Leipziger, J 2018, ' Hydrochlorothiazide and acute urinary acidification : The 'voltage hypothesis' of ENaC-dependent H+ secretion refuted ', Acta Physiologica, vol. 223, no. 1, e13013 . https://doi.org/10.1111/apha.13013
AIM: The 'voltage hypothesis' of H+ secretion states that urinary acidification following increased Na+ delivery to the collecting duct (CD) is ENaC-dependent leading to transepithelial voltage-dependent increase in H+ secretion. We recently showed t
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::d142559c5fafc897ebaa1ffe2c815115
https://pure.au.dk/portal/da/publications/hydrochlorothiazide-and-acute-urinary-acidification(b9f3f2b0-3d56-4623-bbf3-274f0b2cc1fc).html
https://pure.au.dk/portal/da/publications/hydrochlorothiazide-and-acute-urinary-acidification(b9f3f2b0-3d56-4623-bbf3-274f0b2cc1fc).html