Renal effects of the serine protease inhibitor aprotinin in healthy conscious mice
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F. Artunc | C. Daniel | K. Amann | A. Birkenfeld | A. Janessa | B. Bohnert | M. Wörn | M. Xiao | S. Wörner | Bernhard N. Bohnert | Matthias Wörn
[1] F. Artunc,et al. Zymogen‐locked mutant prostasin (Prss8) leads to incomplete proteolytic activation of the epithelial sodium channel (ENaC) and severely compromises triamterene tolerance in mice , 2021, Acta physiologica.
[2] M. Ueffing,et al. Proteasuria in nephrotic syndrome-quantification and proteomic profiling. , 2020, Journal of proteomics.
[3] Ulrich Dirnagl,et al. The ARRIVE guidelines 2.0: Updated guidelines for reporting animal research* , 2020, Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism.
[4] Ulrich Dirnagl,et al. The ARRIVE guidelines 2.0: Updated guidelines for reporting animal research* , 2020, BMC Veterinary Research.
[5] F. Artunc,et al. Plasminogen deficiency does not prevent sodium retention in a genetic mouse model of experimental nephrotic syndrome , 2020, Acta physiologica.
[6] D. Eaton,et al. Regulating ENaC's gate. , 2019, American journal of physiology. Cell physiology.
[7] F. Artunc,et al. Urokinase‐type plasminogen activator (uPA) is not essential for epithelial sodium channel (ENaC)‐mediated sodium retention in experimental nephrotic syndrome , 2019, Acta physiologica.
[8] F. Artunc,et al. Proteasuria—The impact of active urinary proteases on sodium retention in nephrotic syndrome , 2019, Acta physiologica.
[9] C. Yoshioka,et al. Structure of the human epithelial sodium channel by cryo-electron microscopy , 2018, eLife.
[10] K. Bamberg,et al. Na restriction activates epithelial Na channels in rat kidney through two mechanisms and decreases distal Na+ delivery , 2018, The Journal of physiology.
[11] M. Barman,et al. Safety of Perioperative Aprotinin Administration During Isolated Coronary Artery Bypass Graft Surgery: Insights From the ART (Arterial Revascularization Trial) , 2018, Journal of the American Heart Association.
[12] R. Hughey,et al. Epithelial Na+ Channel Regulation by Extracellular and Intracellular Factors. , 2018, Annual review of physiology.
[13] F. Artunc,et al. Aprotinin prevents proteolytic epithelial sodium channel (ENaC) activation and volume retention in nephrotic syndrome. , 2018, Kidney international.
[14] Neal S. Gerstein,et al. Antifibrinolytic Agents in Cardiac and Noncardiac Surgery: A Comprehensive Overview and Update. , 2017, Journal of cardiothoracic and vascular anesthesia.
[15] F. Lang,et al. SGK1-dependent ENaC processing and trafficking in mice with high dietary K intake and elevated aldosterone. , 2017, American journal of physiology. Renal physiology.
[16] E. Hummler,et al. The function and regulation of acid‐sensing ion channels (ASICs) and the epithelial Na+ channel (ENaC): IUPHAR Review 19 , 2016, British journal of pharmacology.
[17] R. Hughey,et al. Prostasin interacts with the epithelial Na+ channel and facilitates cleavage of the γ-subunit by a second protease. , 2014, American journal of physiology. Renal physiology.
[18] J. Chao,et al. Tissue kallikrein activation of the epithelial Na channel. , 2012, American journal of physiology. Renal physiology.
[19] R. Hughey,et al. ENaC at the Cutting Edge: Regulation of Epithelial Sodium Channels by Proteases* , 2009, The Journal of Biological Chemistry.
[20] D. Royston,et al. Aprotinin and renal dysfunction , 2008 .
[21] R. Martineau,et al. A comparison of aprotinin and lysine analogues in high-risk cardiac surgery. , 2008, The New England journal of medicine.
[22] W. White,et al. The effect of aprotinin on outcome after coronary-artery bypass grafting. , 2008, The New England journal of medicine.
[23] K. Zacharowski,et al. Effect of aprotinin on renal dysfunction in patients undergoing on-pump and off-pump cardiac surgery: a retrospective observational study , 2008, The Lancet.
[24] D. Royston,et al. Aprotinin and renal dysfunction. , 2008, Expert opinion on drug safety.
[25] O. Weisz,et al. Epithelial Na+ Channels Are Fully Activated by Furin- and Prostasin-dependent Release of an Inhibitory Peptide from the γ-Subunit* , 2007, Journal of Biological Chemistry.
[26] A. Hoeft,et al. Mortality associated with aprotinin during 5 years following coronary artery bypass graft surgery. , 2007, JAMA.
[27] I. C. Tudor,et al. The risk associated with aprotinin in cardiac surgery. , 2006, The New England journal of medicine.
[28] T. Jentsch,et al. The ClC-5 chloride channel knock-out mouse – an animal model for Dent's disease , 2002, Pflügers Archiv.
[29] C. O'Connor,et al. The impact of renal dysfunction on aprotinin pharmacokinetics during cardiopulmonary bypass. , 1999, Anesthesia and analgesia.
[30] E. Oestreicher,et al. Cellular Distribution of Exogenous Aprotinin in the Rat Kidney , 1998, Biological chemistry.
[31] B. Rossier,et al. An epithelial serine protease activates the amiloride-sensitive sodium channel , 1997, Nature.
[32] J. Ménard,et al. Calcium blockade versus ACE inhibition in clipped and unclipped kidneys of 2K-1C rats. , 1994, Kidney international.
[33] A. E. El Nahas,et al. Role of growth hormone in the development of experimental renal scarring. , 1991, Kidney international.
[34] A. Nasjletti,et al. Segmental nephron function in rats treated with aprotinin, an inhibitor of kallikrein. , 1986, The Journal of pharmacology and experimental therapeutics.
[35] O. Carretero,et al. The effect of aprotinin (a serine protease inhibitor) on renal function and renin release. , 1983, Hypertension.
[36] S. Spitzer,et al. The potassium-sparing and natriuretic activity of N-amidino-3,5-diamino-6-chloropyrazinecarboxamide hydrochloride dihydrate (amiloride hydrochloride). , 1967, Journal of Pharmacology and Experimental Therapeutics.