[On the function of beta3-adrenoceptors in the human heart: signal transduction, inotropic effect and therapeutic prospects].

Beta-adrenergic stimulation is an important regulatory mechanism of cardiac function. Next to beta1- and beta2-adrenoceptors, the expression of a third beta-adrenoceptor population, the beta3-adrenoceptor, has recently been evidenced in the human heart. Stimulation of cardiac beta3-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 beta3-adrenergic stimulation. In both nonfailing and failing myocardium, beta3-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 beta3-adrenoceptor is discussed as a possible target for the pharmacological therapy of heart failure.