Early environmental conditions may set patterns in the fetus and neonate that may permanently change body structure and physiology, leading to cardiovascular and renal disease in later life. The reninangiotensin system(RAS) has known importance for normal renal development, and the adult is modulated both by Na+ and protein intake. However, the influence of maternal Na+ or protein intake on the fetal and newborn intrarenal RAS is unknown. To examine this, we compared renal renin mRNA in newborn offspring of dams maintained on (1) either low protein intake (5% or 8.5%) or normal protein intake (19%) during pregnancy or (2) either high Na+ (3.15%) or normal Na+ diet (0.2%) during pregnancy and lactation. After weaning, diets for littermates surviving to adult life were normal for both protein and Na+ content. Northern blots were performed on total renal RNA, hybridized to renin cDNA, normalized to GAPDH cDNA, and subjected to densitometry. Maternal low protein diet was associated with significant reduction in neonatal intrarenal renin mRNA levels by >99%, 75%, 33% and 33% at 1, 5, 10 and 15 days of age, respectively, p <0.05. Maternal high salt diet suppressed neonatal intrarenal renin mRNA levels by 74%, 44%, and 34% at 0, 5, and 10 days, respectively, p < 0.05. In chronically instrumented littermates at 21 weeks of age, mean arterial pressure was higher than in controls (126±1 cf. 136±1 mmHg in low protein offspring and 124±1 cf. 136±3 mmHg in high salt offspring, p < 0.05). Thus, intrarenal renin mRNA appears to be downregulated both by maternal low protein and high sodium intake. Additionally, same-cohort littermates exposed to maternal low protein or high salt intake in fetal and neonatal life have significantly higher arterial blood pressure as adults. We postulate that early downregulation of the RAS may be associated with impaired renal development and a decreased number of glomeruli, in turn leading to reduced renal function and arterial hypertension later in life.