β -adrenergic receptor kinase 1 (β ARK 1 ) participates in the desensitization of β -adrenergic receptors by uncoupling the signal transduction. The present study was designed to examine whether neurohumoral increase is crucial for the activation of β ARK 1 in heart failure. Four weeks after the ligation of rat coronary artery, LV dP/d t max was reduced, cardiac response to isoproterenol was impaired, and ratio of right ventricular weight to body weight, an index of cardiac hypertrophy, was increased. At the same time,β ARK 1 expression and activity were augmented in the hypertrophied hearts. In addition, plasma norepinephrine content was enhanced in accordance with cardiac hypertrophy, cardiac β ARK 1 expression, LV dP/d t max, and LVEDP. These results of the present study suggest that β ARK 1 is augmented in concert with circulating norepinephrine level and that β ARK 1 may account for, at least in part, the cardiac dysfunction in rat with myocardial infarction.