Dexamethasone reverses the labor-associated myometrial desensitization to beta-adrenergic agonists in the rat.

Abstract

The purpose of our study was to determine the susceptibility of the myometrium to beta-adrenergic agonist-induced desensitization and to determine the ability of dexamethasone to prevent this homologous desensitization. Myometrial tissue was collected from nonpregnant, pregnant, and postpartum rats (n > or = 6) 12 hours after injection of either dexamethasone (0.25 mg subcutaneously) or vehicle (corn oil). The ability of isoproterenol to induce and maintain inhibition of contractile activity was determined in vitro. In addition, the density and affinity of beta-adrenergic receptors was estimated by ligand binding and Scatchard analysis. Dexamethasone significantly increased both the duration of myometrial responsiveness to isoproterenol and the beta-adrenergic receptor number at parturition, but not at other time points. Regardless of pretreatment, the susceptibility of the myometrium to beta-agonist-induced desensitization was greatest around the time of delivery. In the rat, beta-adrenergic agonists are least effective in maintaining myometrial inhibition peripartum, although their effectiveness at this time only can be increased by dexamethasone.