Many studies have reported that GRK4 gene variants were associated with an increase salt sensitivity or with an decrease renin hypertension and sodium excretion because it plays a key role in counter-regulation between the dopaminergic and renin–angiotensin aldosterone systems (RAAS) in the renal proximal tubule, which is the site of approximately 70% of the total renal sodium reabsorption.[14, 32, 33] In particular, a genetic model based on GRK4 R65L, GRK4 A142V and GRK4 A486V was 94.4% predictive of salt-sensitive hypertension in humans. This evidence concerns the gene GRK4 and hypertensive disorder.