Ruttner Zoltan, Ivanics Tamas, Slaaf Dick W, Reneman Robert S, Toth Andras, Ligeti Laszló
Semmelweis University, Faculty of Medicine, Institute of Human Physiology and Clinical Experimental Research, Budapest, Hungary.
J Soc Gynecol Investig. 2002 Sep-Oct;9(5):294-8. doi: 10.1016/s1071-5576(02)00169-7.
It has been well established that oxytocin (OXT) increases intracellular free calcium (Ca(2+)) by targeting both intracellular and extracellular stores, but the mechanisms involved in the increase through activation with prostaglandin F(2alpha) (PGF(2alpha)) are still incompletely understood. This study was designed to elucidate the source(s) of increased Ca(2+) in response to PGF(2alpha) (10(-6) M) or OXT (10(-8) M) administration in the near-term rat myometrium.
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 Ca(2+).
PGF(2alpha) and OXT induced a 30.1% and 35.9%, respectively, increase in developed tension in the potassium chloride-depolarized myometrial strips. Nifedipine reduced the PGF(2alpha) and OXT increased tension by 65.8% and 49.4%, respectively. In vivo, both PGF(2alpha) and OXT increased Ca(2+) in the potassium 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 PGF(2alpha) and OXT by 45.3% and 39.6%.
These findings indicate that in near-term myometrium the source of increased Ca(2+) after administration of PGF(2alpha), similar to OXT, is both extracellular and intracellular.