Prenatal administration of dexamethasone and a low protein diet has been shown to result in hypertension in the offspring when they are adults. The cause for the hypertension is unknown. The purpose of this study was to examine if there was prenatal programming of thick ascending limb transport. Rats were administered either dexamethasone for four days (0.2 mg/kg body weight) by intraperitoneal injection daily between 15th and 18th day of gestation or rats were fed a low protein diet (6% protein) or an isocaloric normal protein diet (20% protein) from day 12 gestation until birth. The offspring were studied as adults. Prenatal dexamethasone and dietary protein deprivation resulted in an increase in blood pressure. Offspring of mothers fed a low protein diet had an increase in medullary but not cortical NKCC2 protein abundance (p<0.01). There was not a statistically significant increase in medullary NKCC2 by prenatal dexamethasone (p=0.07). Both prenatal administration of dexamethasone and a low protein diet resulted in an increase in medullary thick ascending limb chloride transport compared to control (298±33 pmoles/mm•min, 280±26 pmoles/mm•min, and 191±21 pmoles/mm•min, respectively p<0.05). There was a higher lumen positive transepithelial potential difference in the prenatal dexamethasone and low protein group compared to control as well. Administration of furosemide for 24 hours resulted in a decrease in blood pressure in the low protein group but not the control group. This study demonstrates that insults administered to the fetus can program altered sodium transport. Increased tubular sodium transport is a likely cause for the hypertension by prenatal programming.