β-Adrenergic receptors (β-ARs) have a key position not in to the overall regulation of cardiac function and have been shown to play an important role in various cardiac diseases and heart failure in particular. Beta adrenergic receptors (β-ARs) belong to the G protein-coupled receptor (GPCR) superfamily with widespread expression and cardiovascular functions. Three β-AR subtypes (β1-AR, β2-AR, and β3-AR) are expressed in cardiomyocytes. The positive inotropic effect of β-AR stimulation is one of the most effective measures for maintaining cardiac output. The β-AR stimulation induces protein kinase A (PK-A) activation through G protein, adenylyl cyclase (AC) and cyclic adenosine monophosphate (cAMP). PK-A mediated phosphorylation of many calcium-handling molecules enhances ventricular wall motion. However, long term stimulation of these receptors can lead to the deterioration of cardiac function. In addition, the prognosis of heart failure patients improves with β-AR blocking therapy. Prospective, randomized, placebo-controlled outcome trials of β-blockers in heart failure have demonstrated sustained improvements in left ventricular remodeling and significant reductions in mortality and hospitalizations. The clinical evidence for the long-term benefit of β -blocker therapy is so strong that it is now recommended therapy in all patients with Class II or III heart failure symptoms who do not have specific contraindications. Cardiac G protein–coupled receptor kinases are tightly related to the status of β-AR function in the heart and they have lately emerged not only as a potential therapeutic target in HF but also as a biomarker of HF status and response to treatment, potentially useful in HF clinical practice.