Postpartum Abnormalities of Carbohydrate and Cellular Calcium Metabolism in Pregnancy Induced Hypertension

We have previously reported that young, primigravid, African-American women who developed preeclampsia exhibited insulin resistance (elevated fasting insulin:glucose ratios) and abnormal intracellular free calcium ([Ca2+]i) metabolism as early as the second trimester of pregnancy. To determine if these abnormalities persist postpartum (suggesting a genetic link), we evaluated the effects of an oral glucose load (50 g) on plasma and glucose insulin, basal platelet [Ca2+]i and platelet [Ca2+]i responses to arginine vasopressin (AVP). The study population consisted of nine, young, primigravid, African-American women at 43 +/- 12 weeks postpartum from pregnancy induced hypertensive (PIH) gestations and 10 age- and weight-matched African-American women who were 29 +/- 7 weeks postpartum from normal pregnancies. The PIH group consisted of five subjects who were preeclamptic and four subjects with gestational hypertension. Baseline fasting body weights, body mass indices, plasma glucose, plasma insulin, basal platelet [Ca2+]i, and platelet [Ca2+]i responses to AVP were similar in the postpartum PIH and control groups. The oral glucose load had no effect on basal platelet [Ca2+]i levels in either group. However, plasma glucose and insulin and platelet [Ca2+]i responses to AVP were accentuated at 30 min following an oral glucose load suggesting a subtle abnormality of carbohydrate and [Ca2+]i metabolism that persists in individuals with pregnancy induced hypertension. Long term studies involving African-American populations will be necessary to determine if these metabolic abnormalities are associated with an increased propensity to hypertension.