Arginine deficiency and biochemical dysfunction secondary to arginine deficiency are common in pregnancy. Nitric oxide (NO), produced from arginine, influences fetal growth. We tested whether increased availability of L-arg provided through drinking water could improve fetal growth in a model of fetal growth retardation. Pregnant rats reared in a hypobaric hypoxic environment(FiO2.21, 380 mm Hg) develop severe fetal growth retardation (weight at c-section on day 21 of pregnancy: hypoxic: 3.38 ±.70 g, n = 101 fetuses versus normoxic: 5.11 ±.75 g, n = 65 fetuses, p<.000001). Rats maintained in the same hypobaric cage as the hypoxic rats, but who had dietary supplementation with 2% L-arg added to drinking water had improved fetal growth (weight at c-section on day 21 of pregnancy: 4.78 ±.56 g, n = 52 fetuses p<.00001 versus hypoxic; p = NS versus normoxic). D-arginine, unable to induce NO synthesis to the extent of L-arginine, is only partially active at improving fetal growth. Glycine, not known to affect nitric oxide synthesis, does not normalize fetal growth. Rats maintained under hypoxic conditions who had 2% L-arginine added to drinking water had similar protein intake from day 9 to 21 of pregnancy compared to hypoxia treated rats fed normal diets (hypoxic 9.55 ±.92 g per rat, L-arginine supplemented 9.49±.92g per rat). We conclude that dietary L-arg can prevent fetal growth retardation. We speculate that increased dietary arginine leads to increased endogenous NO synthesis, increasing placental blood flow, and improving oxygen and nutrient delivery to the fetus.