The major pathophysiologic derangement is vasospasm. In pregnant women with PIH, an increased sensitivity to the potent vasopressure angiotensin II is noted. This increased sensitivity is noted several weeks before hypertension is seen. The increased peripheral resistance results in constricted plasma volume. Clinically this results in an increase in the hematocrit. With plasma volume constriction, increased peripheral resistance, and arteriolar spasm, endothelial damage occurs and microangiopathic hemolytic anemias and thrombocytopenia can be seen. Maternal-placental perfusion is decreased in PIH and is believed to account for the increased perinatal morbidity and mortality. Additional factors which may predispose a pregnant woman to PIH include a reduction in synthesis of the prostaglandin prostacyclin relative to thromboxane, alterations in the synthesis of endothelium-derived relaxing factor, endothelin-1, and nitric acid. Increased cardiac output may also play a role in PIH.