?-Adrenergic receptors in failing human myocardium

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Abstract
In the human heart the β-adrenergic receptor-G-protein-adenylyl cyclase system is the most powerful physiologic mechanism to acutely increase contractility and/or heart rate. In the failing human myocardium β1-adrenergic receptor number is decreased, and this is accompanied by a reduced β1-adrenergic receptor mediated positive inotropic effect. Cardiac β2-adrenergic receptor number may or may not decrease; however, β2-adrenergic receptor mediated positive inotropic effects are also reduced, possibly because the functional activity of myocardial Gi is increased, thereby inhibiting cyclic AMP formation. The aging human heart shows some similarities with the failing human heart: in both settings, of chronic heart failure and age, β-adrenergic receptor mediated effects and all other cyclic AMP dependent effects are depressed and Gi-protein is increased.