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Abnormality of calcium channel inhibitor released from fetal membranes in preterm labor
E M Carroll1, J G Gianopoulos, P L Collins
1Department of Obstetrics and Gynecology, and the Cardiovascular Institute, Loyola University Medical Center, Maywood, Illinois 60153, USA.
Objective:
This study was undertaken to test the hypothesis that an inhibitor of uterine contractions acting at the level of the dihydropyridine receptor of the uterine L -type uterine calcium channel is released in greater amounts from fetal membranes before term than at term.
Study Design:
Endogenous calcium channel inhibitor activity was generated with standardized 25-cm2 surface area fetal membrane samples from the following 4 categories of women: preterm in labor, preterm not in labor, term in labor, and term not in labor. The amount of inhibitor in each membrane category was quantified by means of a competitive binding assay. Inhibition of uterine contractions induced by Bay K 8644 (an L -type calcium channel agonist) was used as another test of endogenous calcium channel inhibitor activity released from fetal membranes of all 4 groups of patients.
Results:
Endogenous calcium channel inhibitor activity was most variable but present in the greatest amount in fetal membranes of women who were preterm not in labor followed by those in women at term not in labor and at term in labor. Fetal membranes from women in preterm labor had the least amount of measured endogenous calcium channel inhibitor activity. Consistent with the competitive binding assay, endogenous calcium channel inhibitor activity from fetal membranes from women who were preterm not in labor, at term not in labor, and at term in labor inhibited Bay K 8644-induced uterine contractions. Fetal membranes from women in preterm labor did not inhibit Bay K 8644-induced contractions. Endogenous calcium channel inhibitor activity was present in the chorion, the decidua, and the placenta, with little activity in the amnion.
Conclusion:
The down-regulation of endogenous calcium channel inhibitor activity with advancing gestation is consistent with a potential role for this inhibitor in maintaining uterine quiescence and in regulating the transition into labor. One possible cause of idiopathic preterm labor may be an abnormally low amount of endogenous calcium channel inhibitor activity in fetal membranes.