Lack of Inducible NO Synthase Reduces Oxidative Stress and Enhances Cardiac Response to Isoproterenol in Mice With Deoxycorticosterone Acetate–Salt Hypertension

Although NO derived from endothelial NO synthase (eNOS) is thought to be cardioprotective, the role of inducible NO synthase (iNOS) remains controversial. Using mice lacking iNOS (iNOS−/−), we studied (1) whether development of hypertension, cardiac hypertrophy, and dysfunction after deoxycorticoste...

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Veröffentlicht in:	Hypertension (Dallas, Tex. 1979) Tex. 1979), 2005-12, Vol.46 (6), p.1355-1361
Hauptverfasser:	Sun, Ying, Carretero, Oscar A, Xu, Jiang, Rhaleb, Nour-Eddine, Wang, Fangfei, Lin, Chunxia, Yang, James J, Pagano, Patrick J, Yang, Xiao-Ping
Format:	Artikel
Sprache:	eng
Schlagworte:	Aldehydes - metabolism Animals Arterial hypertension. Arterial hypotension Biological and medical sciences Blood and lymphatic vessels Blood Pressure Cardiology. Vascular system Cardiotonic Agents - pharmacology Clinical manifestations. Epidemiology. Investigative techniques. Etiology Desoxycorticosterone Experimental diseases Fundamental and applied biological sciences. Psychology Heart Heart - drug effects Heart - physiopathology Heart failure, cardiogenic pulmonary edema, cardiac enlargement Hemodynamics. Rheology Hypertension - chemically induced Hypertension - metabolism Hypertension - physiopathology Hypertrophy, Left Ventricular - chemically induced Isoproterenol - pharmacology Male Medical sciences Mice Mice, Inbred C57BL Mice, Knockout Myocardium - enzymology Nitric Oxide Synthase Type II - deficiency Nitric Oxide Synthase Type II - metabolism Nitric Oxide Synthase Type III - metabolism Oxidative Stress Sodium Chloride Tyrosine - analogs & derivatives Tyrosine - metabolism Vertebrates: cardiovascular system
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