Prenatal dexamethasone exposure leads to high urine angiotensin II excretion at 4 to 8 weeks of age and increases in systolic blood pressure at 8 weeks without a change in plasma or renal angiotensin II levels, suggesting that luminal angiotensin II concentrations may be driving the development of hypertension via increased sodium transport [73]. The gene discussed is AGT; the disease is hypertensive disorder.