Nitric oxide (NO), initially identified as endothelium-derived relaxing factor (EDRF), is a gaso-transmitter with important regulatory roles in the cardiovascular, nervous and immune systems. In the former, this diatomic molecule and free radical gas controls vascular tone and cardiac mechanics, among others. In the cardiovascular system, it is now understood that β-adrenergic receptor (βAR) activation is a key modulator of NO generation. Therefore, it is not surprising that the up-regulation of G protein-coupled receptor kinases (GRKs), in particular GRK2, that restrains βAR activity contributes to impaired cardiovascular functions via alteration of NO bioavailability. This review, will explore the specific interrelation between βARs, GRK2 and NO in the cardiovascular system and their inter-relationship for the pathogenesis of the onset of disease. Last, we will update the readers on the current status of GRK2 inhibitors as a potential therapeutic strategy for heart failure with an emphasis on their ability of rescuing NO bioavailability.

一氧化氮（NO）最初被确定为内皮源性舒张因子（EDRF），是一种气体传导物，在心血管，神经和免疫系统中具有重要的调节作用。在前者中，这种双原子分子和自由基气体可控制血管张力和心脏力学等。在心血管系统中，现在知道β-肾上腺素受体（βAR）激活是NO生成的关键调节剂。因此，抑制βAR活性的G蛋白偶联受体激酶（GRKs），特别是GRK2的上调，通过改变NO生物利用度，会导致心血管功能受损，这一点不足为奇。这篇评论将探讨βAR之间的具体相互关系，心血管系统中的GRK2和NO及其与疾病发病机理的相互关系。最后，我们将向读者介绍GRK2抑制剂的现状，将其作为心力衰竭的潜在治疗策略，重点是其挽救NO生物利用度的能力。