Lymphocyte intracellular free calcium concentration is increased in preeclampsia

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Abstract

OBJECTIVES

We tested 2 hypotheses: (1) Preeclampsia is characterized by an increase in intracellular free calcium concentration in lymphocytes. (2) Levels of intracellular free calcium are influenced by the calcium concentration in the extracellular milieu or by parathyroid hormone.

STUDY DESIGN

Intracellular free calcium concentrations were measured in 4 groups of women: nonpregnant women (n = 25), normotensive pregnant women (n = 30), pregnant women with chronic hypertension (n = 15), and women with preeclampsia (n = 15). Intracellular free calcium concentration was measured in the basal state, at varying extracellular calcium ion concentrations, and in the presence of exogenous parathyroid hormone.

RESULTS

Women with preeclampsia had the highest basal lymphocyte intracellular free calcium concentration (121 +/- 7 nmol/L, mean +/- SEM) compared with normotensive pregnant women during the third trimester (94 +/- 3 nmol/L, P < .001) and pregnant women in the third trimester with chronic hypertension (100 +/- 3 nmol/L, P < .01). During the third trimester normotensive women and women with chronic hypertension had significantly higher basal intracellular free calcium concentrations than were found in women during the first trimester. Exposure of lymphocytes to an extracellular milieu of low calcium concentration resulted in an increase in intracellular free calcium concentration. Incubation with parathyroid hormone had no effect on intracellular free calcium concentration.

CONCLUSIONS

Lymphocyte intracellular free calcium concentration is increased in preeclampsia and not in chronic hypertensive pregnancy and is greater during the third trimester than during the first trimester. Extracellular calcium depletion increases lymphocyte intracellular free calcium concentration. These data support the idea that a calcium deficit leading to an increased intracellular free calcium concentration during late pregnancy contributes to the pathogenesis of preeclampsia. (Am J Obstet Gynecol 1999;180:1209-14.)

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