The success of Angiotensin II receptor blockers, specifically Angiotensin II type 1 receptor (AT1R) antagonists as antihypertensive drug emphasizes the involvement of AT1R in Essential hypertension. The structural insights and mutational studies of Ang II-AT1R have brought about the vision to design Ang II analogs that selectively activate the pathways with beneficial and cardioprotective effects such as cell survival and hinder the deleterious effects such as hypertrophy and cell death. AT1R belongs to G-protein coupled receptors and is regulated by G-protein coupled receptor kinases (GRKs) that either uncouples Gq protein for receptor desensitization or phosphorylate C-terminus to recruit β-arrestin for internalization of the receptor. The interaction of GRKs with ligand activated AT1R induces conformational changes and signal either Gq dependent or Gq independent pathways. These interactions might explain the complex regulatory mechanisms and offer promising ideas for hypertension therapeutics. This article reviews the functional role of AT1R, organization of GRK genes and regulation of AT1R by GRKs that play significant role in desensitization and internalization of the receptors.

血管紧张素 II 受体阻滞剂，特别是血管紧张素 II 1 型受体 (AT1R) 拮抗剂作为抗高血压药物的成功强调了 AT1R 与原发性高血压的关系。 Ang II-AT1R 的结构见解和突变研究带来了设计 Ang II 类似物的愿景，该类似物选择性地激活具有有益和心脏保护作用（如细胞存活）的途径，并阻止有害作用（如细胞肥大和细胞死亡）。 AT1R 属于 G 蛋白偶联受体，受 G 蛋白偶联受体激酶 (GRK) 调节，GRK 解偶联 Gq 蛋白以实现受体脱敏，或磷酸化 C 末端以募集 β-抑制蛋白以实现受体内化。 GRK 与配体激活的 AT1R 的相互作用诱导构象变化并发出 Gq 依赖性或 Gq 独立途径的信号。这些相互作用可能解释复杂的调节机制，并为高血压治疗提供有希望的想法。本文综述了 AT1R 的功能作用、GRK 基因的组织以及 GRK 对 AT1R 的调节，这些在受体脱敏和内化中发挥着重要作用。