Abstract-Fetal malnutrition and hypoxia may modify organ system maturation and result in cardiovascular diseases in the adult. We tested whether intrauterine stress (IUS) leads to persistent alterations of renal biology. In rats, intrauterine stress was induced by ligation of the uterine arteries at day 17 of pregnancy. Renal arteries of the 21-day-old male offspring were isolated to study pharmacological reactivity. Kidneys were dissected to analyze renal structure and -adrenoceptor expression. At 21 days of age, half of the animals underwent unilateral left nephrectomy. At the age of 12 weeks, rats were instrumented for blood pressure monitoring, blood sampling, and renal function measurements. After IUS, litter size and birth weight were reduced, whereas the hematocrit was increased. Renal arterial responses to -adrenergic stimulation and sensitivity to adenylyl cyclase activation were increased, along with the renal expression of  2 -adrenoceptors. At 21 days and at 6 months of age, the number and density of the glomeruli were reduced, whereas their size was increased. The filtration fraction and urinary albumin concentration were increased 12 weeks after intrauterine stress. In control rats, removal of the left kidney at 21 days of age did not affect kidney function and blood pressure. However, after IUS, the remaining right kidney failed to compensate for the loss of the left kidney, and blood pressure was increased. In conclusion, prenatal stress transiently modifies renal arterial reactivity and results in long-lasting adverse effects on renal structure and function and on renal compensatory mechanisms. Key Words: hypertension Ⅲ kidney Ⅲ glomerular filtration rate Ⅲ nephrectomy Ⅲ pregnancy Ⅲ rats Ⅲ renal artery Ⅲ receptors, adrenergic beta C ardiovascular, endocrine and metabolic diseases can emerge as a consequence of intrauterine stress (IUS). 1 A suboptimal fetal environment is often the result of placental insufficiency, which leads to an inadequate delivery of nutrients and oxygen to the fetus. Many animal models have been established that support a link between prenatal conditions and the development of disease in the adult. These include maternal caloric and protein restriction, 2 exposure to hypoxia, 3 and ligation of the uterine arteries to mimic placental insufficiency. 4 Hypoxia and malnutrition during fetal life were reported to affect the renin-angiotensin system, the hypothalamicpituitary-adrenal axis, 5 vascular endothelial function and sympathetic innervation, 3,4,6 and the development of organs like the kidney. 7 The number of glomeruli can be permanently reduced by influences during fetal life. These structural changes may contribute to renal dysfunction 8 and hypertension 9 later in life. Other aspects of renal organogenesis, such as renal vascular development and particularly adrenoceptor-mediated renovascular responses, 10 might also be influenced by disturbed fetal growth. In the rat, an unfavorable intrauterine environment, induced by uterine artery ligation, modified postnatal ...