dimethylarginine dimethylaminohydrolase1 is an organ-specific mediator of end organ damage in a murine model of hypertensiondimethylarginine dimethylaminohydrolase1是结束的瀑特异性中介器官损伤小鼠模型的高血压.pdfVIP

Dimethylarginine Dimethylaminohydrolase1 Is an Organ-Specific Mediator of End Organ Damage in a Murine Model of Hypertension 1 1 1 2 1 Karsten Sydow *, Christine Schmitz , Eike-Christin von Leitner , Robin von Leitner , Anna Klinke , 3 2 1 4 3 Dorothee Atzler , Christian Krebs , Hartwig Wieboldt , Heimo Ehmke , Edzard Schwedhelm , 1 1 ¨ 3 5 1. Thomas Meinertz , Stefan Blankenberg , Rainer H. Boger , Tim Magnus , Stephan Baldus , Ulrich Wenzel2. 1 Department of Interventional Cardiology, Hamburg University Heart Center, University Hospital Hamburg-Eppendorf, Hamburg, Germany, 2 Department of Nephrology, University Hospital Hamburg-Eppendorf, Hamburg, Germany, 3 Institute of Clinical Pharmacology and Toxicology, University Hospital Hamburg-Eppendorf, Hamburg, Germany, 4 Institute of Cellular and Integrative Physiology, University Hospital Hamburg-Eppendorf, Hamburg, Germany, 5 Department of Neurology, University Hospital Hamburg-Eppendorf, Hamburg, Germany Abstract Background: The endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) is an independent predictor of cardiovascular and overall mortality. Moreover, elevated ADMA plasma concentrations are associated with the extent of hypertension. However, data from small-sized clinical trials and experimental approaches using murine transgenic models have revealed conflicting results regarding the impact of ADMA and its metabolizing enzyme dim