Summary
β-adrenergic stimulation is an important regulatory mechanism of cardiac function. Next to β1- and β2-adrenoceptors, the expression of a third β-adrenoceptor population, the β3-adrenoceptor, has recently been evidenced in the human heart. Stimulation of cardiac β3-adrenoceptors leads to a decrease in contractility via a release of nitric oxide (NO). In this context, different molecular mechanisms of endothelial nitric oxide synthase (eNOS) activation have been uncovered to occur as a consequence of β3-adrenergic stimulation. In both nonfailing and failing myocardium, β3-adrenergic stimulation may have a protective effect against excessive chatecolaminergic stimulation as it occurs during somatic and mental stress and during heart failure. For this reason, the β3-adrenoceptor is discussed as a possible target for the pharmacological therapy of heart failure.