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Is the attenuation of beta-adrenergic agonist efficacy during labor caused by elevated prostaglandin E levels?
S J Lye1, P Bernstein, M Oskamp
1Program in Development and Fetal Health, Samuel Lunenfeld Research Institute, Department of Obstetrics and Gynaecology, Mount Sinai Hospital, University of Toronto, Toronto, Ontario, Canada.
Objective:
Our purpose was to investigate whether attenuation of beta-adrenergic agonist efficacy during labor is due to elevated prostaglandin E levels.
Study Design:
beta-Receptor function (response to beta-agonist or forskolin) was tested in mononuclear leukocytes collected from women at term before or during labor. beta-Receptor function was also tested in mononuclear leukocytes of nonlaboring patients after in vitro incubation with oxytocin (1 micromol/L), prostaglandin E2 (10 micromol/L), prostaglandin F2alpha (10 micromol/L), or buffer alone.
Results:
Mononuclear leukocytes from women in active labor exhibited a significant attenuation of beta-adrenergic receptor function as a result of reduced adenylyl cyclase activity. This effect could be induced in mononuclear leukocytes from nonlaboring women by preincubation with prostaglandin E but not oxytocin or prostaglandin F.
Conclusions:
Prostaglandin E induces heterologous desensitization of the beta-adrenergic receptor system in mononuclear leukocytes, comparable to that seen during labor. We speculate that during labor the elevated levels of prostaglandin E may induce similar effects on the myometrium, thereby decreasing the efficacy of beta-agonists as tocolytics.