Selective Endothelin ETB Receptor Antagonist Improves Left Ventricular Function but Exaggerates Degeneration of Cardiomyocytes in J 2 Nk Hamsters

ET-1 may act as a potent growth factor inducing cardiac hypertrophy, 3 and exert positive inotropic and chronotropic effects on the heart. 4,5 Moreover, extremely elevated concentrations of ET-1 might be toxic and cause local myocyte damage, leading to cardiac dysfunction. 6 Although both ETA receptor-selective antagonist and nonselective ETA/ETB receptor antagonist have been reported to improve cardiac function in CHF, it is still controversial whether selective ETA receptor blockade or nonselective ETA/ETB receptor blockade is preferable for the treatment of patients with CHF, because the pathophysiological role of ETB receptors in CHF has not been fully elucidated.7–10 Furthermore, little is known about the effect of long-term treatment with ETB receptor blockade on cardiac function and structure in CHF.