G protein-coupled receptors (GPCRs) mediate cellular responses to diverse extracellular stimuli that play vital roles in the regulation of biology, including behavior. Abnormal G protein-coupled receptor kinase (GRK)-mediated regulation of GPCR function is involved in the pathogenesis of hypertension. Among the seven GRK subtypes, GRK4 has attracted attention because of its constitutive activity and tissue-specific expression. Increasing number of studies show that GRK4 affects blood pressure by GPCR-mediated regulation of renal and arterial function. The target receptor of GRK4 is confined not only to GPCRs, but also to other blood pressure-regulating receptors, such as the adiponectin receptor. Genetic studies in humans show that in several ethnic groups, GRK4 gene variants (R65L, A142V, and A486V) are associated with salt-sensitive or salt-resistant essential hypertension and blood pressure responses to antihypertensive medicines. In this article, we present a comprehensive overview of GRK-mediated regulation of blood pressure, focusing on the latest research progress on GRK4 and hypertension and highlighting potential and novel strategies for the prevention and treatment of hypertension.

G 蛋白偶联受体 (GPCR) 介导细胞对多种细胞外刺激的反应，在包括行为在内的生物学调节中发挥重要作用。G 蛋白偶联受体激酶 (GRK) 介导的 GPCR 功能异常调节参与高血压的发病机制。在七种GRK亚型中，GRK4因其组成型活性和组织特异性表达而引起人们的关注。越来越多的研究表明，GRK4 通过 GPCR 介导的肾功能和动脉功能调节来影响血压。GRK4的靶受体不仅限于GPCR，还包括其他血压调节受体，例如脂联素受体。人类遗传学研究表明，在几个种族群体中，GRK4基因变异（R65L、A142V 和 A486V）与盐敏感或耐盐原发性高血压以及抗高血压药物的血压反应有关。在本文中，我们对GRK介导的血压调节进行了全面概述，重点介绍了GRK4与高血压的最新研究进展，并重点介绍了预防和治疗高血压的潜在和新颖策略。