Uterine blood supply is a critical issue for fetal well-being, since it carries all the nutrients, including O₂, required for fetal growth and gets rid of several fetal waste products. During pregnancy, uterine blood flow increases by almost 20 times and this is permitted by marked remodeling of the vessel wall. In the rat, uterine arterial remodeling takes place in the last 7–8 days of gestation (over 22) and is reversible in the postpartum period upon a similar time frame. It was also described as both hypertrophy and hyperplasia of all the constituents of the vascular wall. Several hypotheses have been proposed to explain such a phenomenon, including the driving role not only of sexual steroid hormones, progesterone and estrogens, but also of trophic factors of fetal origin. We have shown that alterations of the renin–angiotensin–aldosterone system, by manipulating sodium intake in the rats, reduced the pregnancy-induced remodeling of uterine arteries. These maneuvres resulted in the birth of pups that had characteristics of intrauterine growth restriction or in the development in the mother of “experimental” gestational hypertension, depending on, respectively, restriction or increased of sodium intake.