β-Adrenergic receptors (βARs) belong to a large family of cell surface receptors known as G protein-coupled receptors (GPCRs). They are coupled to Gs protein (Gαs) for the activation of adenylyl cyclase (AC) yielding cyclic AMP (CAMP), and this provides valuable responses, which can affect the cardiac function such as injury. The binding of an agonist to βAR enhances conformation changes that lead to the Gαs subtype of heterotrimeric G protein which is the AC stimulatory G protein for activation of CAMP in the cells. However, cardiovascular diseases (CVD) have been reported as having an increased rate of death and β1AR, and β2AR are a promising tool that improves the regulatory function in the cardiovascular system (CVS) via signaling. It increases the Gα level, which activates βAR kinase (βARK) that affects and enhances the progression of heart failure (HF) through the activation of cardiomyocyte βARs. We also explained that an increase in GPCR kinases (GRKs) would practically improve the HF pathogenesis and this occurs via the desensitization of βARs, which causes the loss of contractile reserve. The consistency or overstimulation of catecholamines contributes to CVD such as stroke, HF, and cardiac hypertrophy. When there is a decrease in catecholamine responsiveness, it causes aging in old people because the reduction of βAR sensitivity and density in the myocardium enhances downregulation of βARs to AC in the human heart.
Keywords: Adenylyl cyclase; Cardiovascular disease; Catecholamines; GPCR; Heart failure; β-Adrenergic receptor.