In GS, Na+/Cl− co-transporter (NCC) and ENaC activity is enhanced, paracellular Cl− reabsorption is further increased, and renal outer medullary K+ channel (ROMK) activity is further decreased, leading to increased salt reabsorption and decreased K+ excretion, and therefore to hypertension and hyperkalemia, respectively. This evidence concerns the gene SLC12A3 and hypertensive disorder.