A rat model of hypertension induced by in utero exposure to maternal low protein diets has previously been described. Low protein exposed rat pups are of lower weight at birth and have large associated placentas. Such animals are proposed, therefore, to mirror individuals in the human population perceived to be at greater risk of cardiovascular disease in adulthood. Recent work has suggested that maternal glucocorticoids may programme this increased risk of later disease. The role of glucocorticoids in programming the hypertensive state was assessed by administration of the 11β-hydroxylase inhibitor, metyrapone, to pregnant rats consuming 18 (control) or 9% (low protein) casein diets. At day 14 of pregnancy, fetuses and placentas of low protein-fed rats were significantly larger than those of controls. Metyrapone significantly inhibited corticosterone synthesis in both dietary groups, and attenuated the more rapid growth of fetus and placenta in the low protein fed group. Systolic blood pressures of rats exposed to the low protein diet in utero were significantly higher (29 mmHg) than those exposed to the control diet. Metyrapone abolished the hypertensive state of low protein exposed rats, but in the control group significantly elevated blood pressure by 15 mm Hg. Maternal and fetal glucocorticoid interactions in utero clearly have an important role in determining future regulation of blood pressure. Maternal-diet induced hypertension in the rat would appear to be a glucocorticoid-dependent phenomenon.