Objective G-protein-coupled receptor kinase 4 (GRK4) negatively regulates sodium balance in the proximal tubule of the kidney by desensitizing the dopamine-1-receptor. It is reported that mutation of GRK4 gene has been linked to impaired natriuresis and hypertension. In the current paper, we establish GRK4γ wild-type and three GRK4γvariant transgenic mice and analyze dynamic blood pressure using this transgenic mouse model. Methods The transgenic vector was constructed by inserting the human GRK4γ wild-type, GRK4γR65L, GRK4γA142V and GRK4γA486V gene into the down steam of chickenβ-actin promoter respectively. The transgenic mice were created by the method of microinjection. The genotype of transgenic line was identified by PCR and the expression level of target gene was determined by Western blot. Dynamic blood pressure was measured by noninvasive blood pressure meter. Results Each line of human wild-type, GRK4γR65L, GRK4γA142V and GRK4γA486V C57BL/6J transgenic mice with high levels of GRK4 expression in heart, kidney and adrenal gland tissues was established. Mice overexpressing the human GRK4γ wild-type and GRK4γR65L gene are normotensive, whereas mice overexpressing the human GRK4γA142V are hypertensive even on a normal NaCl intake. In contrast, human GRK4γA484V transgenic mice become hypertensive only after an increase in sodium intake. Conclusion GRK4γA142V transgenic mice could be an animal model for spontaneous hypertension, whereas GRK4γA486V transgenic mice could be an animal model for salt-sensitive hypertension.