Pott C, Brixius K, Bloch W, Ziskoven C, Napp A, Schwinger R H G
Laboratory for Muscle Research and Molecular Cardiology, Department of Internal Medicine III, University of Cologne, Germany.
Pharmazie. 2006 Apr;61(4):255-60.
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.
除β1-和β2-肾上腺素能受体外，人类心脏中还表达了第三种肾上腺素能受体亚型，即β3-肾上腺素能受体。在哺乳动物心室肌细胞中，β3-肾上腺素能刺激通过释放一氧化氮（NO）导致收缩力下降。最近，在心肌细胞中发现了β3-肾上腺素能激活内皮型一氧化氮合酶（eNOS）的不同分子机制。在非衰竭心脏尤其是衰竭心脏中，β3-肾上腺素能刺激可能提供保护，防止过度的儿茶酚胺能β1-肾上腺素能受体刺激。在这种情况下，β3-肾上腺素能受体被视为心力衰竭药物治疗的新靶点。
