shows that EP4 may be involved in the pathogenesis of hyperprostaglandin E syndrome/antenatal Bartter syndrome (HPS/aBS), and gene target disruption of EP4-/- on mixed background mice suppresses furosemide induced diuresis and electrolyte excretion, suggesting a natriuretic role of EP4 (70). Here, PTGER4 is linked to Bartter disease type 1.