The etiology of preeclampsia is not known. There are some partial well established mechanisms like decreased refractoriness to vasoactive agents, reduced placental and artery wall production of prostacyclin, increased production of thromboxane, and luminal trophoblast invasion of spiral arteries. We propose that it would be of primary importance to elucidate the role of uterine artery as an early pathway of preeclamptic disease. Defective hypertrophy of the uterine artery during pregnancy may give way to stretching, distortion and narrowing of the arterial lumen. The rate of growth of the pregnant uterus may not be synchronous with the expected hypertrophy of the uterine artery, thus jeopardizing the blood flow in its branches, such as arcuate and spiral arteries. This disturbance may cause non invasion by the trophoblast of the spiral arteries and subsequent placental hypoxia. Exaggerated uterine volume, like multiple pregnancy, hydatiform mole and hydramnios, may facilitate preeclampsia by demanding more blood supply from an inadequate uterine artery. The prevalence of preeclampsia in primiparous women can be understood, since additional pregnancies will find the uterine arteries already elongated, at least to some extent.