Endothelin-A receptor blockade prevents left ventricular hypertrophy and dysfunction in salt-sensitive experimental hypertension

Salt-sensitive hypertension represents a major cause of left ventricular (LV) dysfunction. We therefore explored the potential effects of the selective endothelin-A (ETA) receptor antagonist darusentan on the development of hypertension, LV hypertrophy (LVH), and dysfunction in a genetic rat model o...

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Veröffentlicht in:	Circulation (New York, N.Y.) N.Y.), 2002-10, Vol.106 (18), p.2305-2308
Hauptverfasser:	Rothermund, Lars, Vetter, Roland, Dieterich, Maike, Kossmehl, Peter, Gögebakan, Ozlem, Yagil, Chana, Yagil, Yoram, Kreutz, Reinhold
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Atrial Natriuretic Factor - genetics Atrial Natriuretic Factor - metabolism Blood Pressure - drug effects Calcium-Binding Proteins - metabolism Calcium-Transporting ATPases - metabolism Desoxycorticosterone Disease Models, Animal Endothelin Receptor Antagonists Fibrosis - etiology Heart Ventricles - drug effects Heart Ventricles - metabolism Heart Ventricles - pathology Hypertension - chemically induced Hypertension - complications Hypertension - drug therapy Hypertension - genetics Hypertrophy, Left Ventricular - etiology Hypertrophy, Left Ventricular - pathology Hypertrophy, Left Ventricular - prevention & control Male Organ Size - drug effects Phenylpropionates - pharmacology Pyrimidines - pharmacology Rats Rats, Inbred Strains Receptor, Endothelin A RNA, Messenger - biosynthesis Sarcoplasmic Reticulum Calcium-Transporting ATPases Sodium Chloride Ventricular Dysfunction, Left - diagnosis Ventricular Dysfunction, Left - etiology Ventricular Dysfunction, Left - prevention & control
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