Induction of Cardiac β -adrenergic Receptor Kinase 1 in Rat Heart Failure Caused by Coronary Ligation

β -adrenergic receptor kinase 1 (β ARK1) 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 ARK1in 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 ARK1expression and activity were augmented in the hypertrophied hearts. In addition, plasma norepinephrine content was enhanced in accordance with cardiac hypertrophy, cardiac β ARK1expression, LV dP/d t max, and LVEDP. These results of the present study suggest that β ARK1is augmented in concert with circulating norepinephrine level and that β ARK1may account for, at least in part, the cardiac dysfunction in rat with myocardial infarction.