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Beta2-adrenoceptor desensitization in non-pregnant estrogen-primed rat myometrium involves modulation of oxytocin

T Engstrøm1, P Bratholm, H Vilhardt

  • 1Department of Internal Medicine and Endocrinology, Herlev Hospital, University of Copenhagen, Denmark.

Journal of Molecular Endocrinology
|May 19, 1998
PubMed

Insights

Beta2-adrenoceptor (beta2AR) stimulation can increase oxytocin receptor (OTR) expression in the non-pregnant rat myometrium. This suggests a novel interaction where beta2AR activation up-regulates OTR, impacting uterine contractility.

Area of Science:

  • Reproductive Endocrinology
  • Pharmacology
  • Molecular Biology

Background:

  • Oxytocin (OT) and beta2-adrenoceptor (beta2AR) agonists have opposing effects on myometrial contractility.
  • Homologous desensitization of these systems is known, but their potential interaction remains unexplored.
  • Understanding these interactions is crucial for managing uterine function, particularly during pregnancy and labor.

Purpose of the Study:

  • To investigate the potential interaction between the oxytocin receptor (OTR) and beta2-adrenoceptor (beta2AR) systems in the non-pregnant rat myometrium.
  • To determine if beta2AR stimulation influences OTR expression or function.
  • To explore the mechanisms underlying homologous desensitization in these systems.

Main Methods:

  • Long-term in vivo treatment of estrogen-primed rats with isoproterenol (a beta2AR agonist) or oxytocin.
  • Assessment of isolated uterine strip contractility and relaxation responses to isoproterenol and oxytocin.
  • Quantification of beta2AR and OTR mRNA levels and OTR binding using molecular and biochemical techniques.

Main Results:

  • Isoproterenol treatment led to homologous desensitization of beta2AR-mediated relaxation, without altering beta2AR mRNA levels.
  • Oxytocin treatment did not affect beta2AR mRNA or isoproterenol-induced relaxation, nor OTR mRNA levels.
  • Isoproterenol treatment significantly increased OTR mRNA, OTR binding, and augmented the contractile response to oxytocin, indicating heterologous up-regulation of OTR.

Conclusions:

  • Beta2AR stimulation in the non-pregnant estrogen-primed rat myometrium leads to a heterologous up-regulation of oxytocin receptors.
  • This up-regulation of OTR is associated with increased receptor number and enhanced uterine contractility in response to oxytocin.
  • Homologous desensitization to beta2 stimulation occurs independently of changes in beta2AR gene expression.

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