Beta3-adrenergic stimulation in the human heart: signal transduction, functional implications and therapeutic perspectives.
Next to beta1- and beta2-adrenoceptors, a third beta-adrenoceptor population is expressed in the human heart, the beta3-adrenoceptor. In mammalian ventricular myocytes, beta3-adrenergic stimulation leads to a decrease in contractility via a release of nitric oxide (NO). Recently, different molecular mechanisms of beta3-adrenergic activation of endothelial nitric oxide synthase (eNOS) have been uncovered in cardiac myocytes. In the non-failing and especially the failing heart, beta3-adrenergic stimulation may offer protection against excessive catecholaminergic beta1-adrenoceptor stimulation. In this context, the beta3-adrenoceptor is discussed as a novel target for the pharmacological therapy of heart failure.
Pott
C
C
Laboratory for Muscle Research and Molecular Cardiology, Department of Internal Medicine III, University of Cologne, Germany.
Brixius
K
K
Bloch
W
W
Ziskoven
C
C
Napp
A
A
Schwinger
R H G
RH
D058667:Adrenergic beta-3 Receptor Agonists; D000318:Adrenergic beta-Agonists / Q000627:therapeutic use*; D006321:Heart / Q000187:drug effects*; D006331:Heart Diseases / Q000188:drug therapy*; D006801:Humans; D015398:Signal Transduction / Q000502:physiology*; D013268:Stimulation, Chemical
D058667:Adrenergic beta-3 Receptor Agonists; D000318:Adrenergic beta-Agonists