Gastrin, by stimulating its receptor, CCKBR,26 exerts a natriuretic effect due to inhibition of NHE activity, such as NHE3.25,41 Gastrin can also induce the expression of its own receptor (CCKBR), which would further amplify cellular CCKBR signaling.42 Genome-wide association studies have shown that the chromosomal loci of CCKBR (11p15.5)43 and GAST (17q21)44 are linked to human essential hypertension.45 Germline deletion of Gast46 or Cckbr27 in mice decreases urine sodium concentration and increases BP. This evidence concerns the gene SLC9A3 and hypertensive disorder.