Objective:
It has been well established that oxytocin (OXT) increases intracellular free calcium ([Ca2+]i) by targeting both intracellular and extracellular stores, but the mechanisms involved in the increase through activation with prostaglandin F2α (PGF2α) are still incompletely understood. This study was designed to elucidate the source(s) of increased [Ca2+]i in response to PGF2α (10-6 M) or OXT (10-8 M) administration in the near-term rat myometrium.
Methods:
The animals were divided into an in vitro group (n = 8), where the developed tension of uterine strips was assessed, and an in vivo group (n = 5), where a lobe of the uterus with intact innervation and circulation was loaded with the fluorescent indicator Indo-1 AM to assess [CA2+]i.
Results:
PGF2α and OXT induced a 30.1% and 35.9%, respectively, increase in developed tension in the potassium chloride-depolarized myometrial strips. Nifedipine reduced the PGF2α and OXT increased tension by 65.8% and 49.4%, respectively. In vivo, both PGF2α and OXT increased [Ca2+]i in the pottassium chloride-depolarized uterine muscle by 35.7% and 44.6%, respectively, increases similar to the rises in tension in vitro. Nifedipine reduced these effects of PGF2α and OXT by 45.3% and 39.6%.
Conclusions:
These findings indicate that in near-term myometrium the source of increased [Ca2+]i after administration of PGF2α, similar to OXT, is both extracellular and intracellular.