Pathophysiology of pregnancy-induced hypertension

Pregnancy-induced hypertension (PIH) is estimated to affect 7% to 10% of al l pregnancies in the United States. Despite being the leading cause of mate rnal death and a major contributor of maternal and perinatal morbidity, the mechanisms responsible for the pathogenesis of PIH have not yet been fully elucidated. Studies during the past decade, however, have provided a bette r understanding of the potential mechanisms responsible for the pathogenesi s of PM. The initiating event in PM appears to be reduced uteroplacental pe rfusion as a result of abnormal cytotrophoblast invasion of spiral arteriol es. Placental ischemia is thought to lead to widespread activation/dysfunct ion of the maternal vascular endothelium that results in enhanced formation of endothelin and thromboxane, increased vascular sensitivity to angiotens in II, and decreased formation of vasodilators such as nitric oxide and pro stacyclin. The quantitative importance of the various endothelial and humor al factors in mediating the reduction in renal hemodynamic and excretory fu nction and elevation in arterial pressure during PIH is still unclear. Inve stigators are also attempting to elucidate the placental factors that are r esponsible for mediating activation/dysfunction of the maternal vascular en dothelium. Microarray analysis of genes within the ischemic placenta should provide new insights into the link between placental ischemia and hyperten sion. More effective strategies for the prevention of preeclampsia should b e forthcoming once the underlying pathophysiologic mechanisms that are invo lved in PIH are completely understood. (C) 2001 American Journal of Hyperte nsion, Ltd.