Characterization of an oxytocin-induced rise in [Ca2+](i) in single human myometrium smooth muscle cells

The effect of the uterotonic pituitary hormone oxytocin on the regulation of intracellular calcium concentration ([Ca2+](i)) was studied in single cells of a smooth muscle cell line derived from human non-pregnant myometrium. [Ca2+](i) was measured with fluorescence microscopy, and by recording the activity of Ca2+-activated potassium currents (I-K(Ca)) on the whole cell and single channel level. Oxytocin induced a rapid and transient increase in [Ca2+](i) that was paralleled by a significant increase in I-K(Ca) activity. After removal of extracellular Ca2+, repetitive stimulation with oxytocin did not alter the [Ca2+](i) transients initially; however, their amplitude became progressively smaller and the response was eventually abolished completely, indicating that oxytocin increased [Ca2+](i) by release of Ca2+ from intracellular stores. Nifedipine did not alter the oxytocin-induced [Ca2+](i)-transients suggesting that oxytocin failed to activate Ca2+ entry through voltage-operated Ca2+ channels. Thapsigargin abolished the oxytocin-induced [Ca2+](i) transient. Caffeine alone had no effect on [Ca2+](i), however it diminished the oxytocin-induced [Ca2+](i) transients. Ryanodine did not affect the oxytocin response indicating that these cells lack release of Ca2+ from the ryanodine receptor release channel, These results demonstrate that oxytocin elicited [Ca2+](i) transients predominantly through Ca2+ release from thapsigargin-sensitive stores, presumably by activating an inositol 1,4,5-trisphosphate dependent pathway.