Jr. Holda et al., CHARACTERIZATION OF AN OXYTOCIN-INDUCED RISE IN [CA2-MUSCLE CELLS(](I) IN SINGLE HUMAN MYOMETRIUM SMOOTH), Cell calcium, 20(1), 1996, pp. 43-51
The effect of the uterotonic pituitary hormone oxytocin on the regulat
ion of intracellular calcium concentration ([Ca2+](i)) was studied in
single cells of a smooth muscle cell line derived from human non-pregn
ant myometrium. [Ca2+](i) was measured with fluorescence microscopy, a
nd by recording the activity of Ca2+-activated potassium currents (I-K
(Ca)) on the whole cell and single channel level. Oxytocin induced a r
apid and transient increase in [Ca2+](i) that was paralleled by a sign
ificant increase in I-K(Ca) activity. After removal of extracellular C
a2+, repetitive stimulation with oxytocin did not alter the [Ca2+](i)
transients initially; however, their amplitude became progressively sm
aller and the response was eventually abolished completely, indicating
that oxytocin increased [Ca2+](i) by release of Ca2+ from intracellul
ar stores. Nifedipine did not alter the oxytocin-induced [Ca2+](i)-tra
nsients suggesting that oxytocin failed to activate Ca2+ entry through
voltage-operated Ca2+ channels. Thapsigargin abolished the oxytocin-i
nduced [Ca2+](i) transient. Caffeine alone had no effect on [Ca2+](i),
however it diminished the oxytocin-induced [Ca2+](i) transients. Ryan
odine did not affect the oxytocin response indicating that these cells
lack release of Ca2+ from the ryanodine receptor release channel, The
se results demonstrate that oxytocin elicited [Ca2+](i) transients pre
dominantly through Ca2+ release from thapsigargin-sensitive stores, pr
esumably by activating an inositol 1,4,5-trisphosphate dependent pathw
ay.