Open AccessOxytocin‐induced oscillations of cytoplasmic Ca 2+ in human myometrial cells
Author(s) -
FU XIN,
LIU YIJIA,
CIRAY NADIR,
OLOVSSON MATTS,
ULMSTEN ULF,
GYLFE ERIK
Publication year - 2000
Publication title -
acta obstetricia et gynecologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.401
H-Index - 102
eISSN - 1600-0412
pISSN - 0001-6349
DOI - 10.1034/j.1600-0412.2000.079003174.x
Subject(s) - myometrium , endocrinology , oxytocin , medicine , intracellular , verapamil , antagonist , inositol , biophysics , calcium , biology , uterus , receptor , biochemistry
Background. To investigate the mechanisms of oxytocin (OT) induced oscillations of the cytoplasmic Ca 2+ concentration ([Ca 2+ ] i ) in cultured human myometrial cells. Methods. [Ca 2+ ] i was measured in individual myometrial cells by dual wavelength spectrophotofluorometry using the fluorescent indicator fura‐2. Myometrium was obtained at abdominal hysterectomy ( n =8) and during cesarean section ( n =7). Results. OT (10–300 nM) typically induced [Ca 2+ ] i oscillations with frequencies in the 0.6–0.8/min range. There were no obvious differences in the responses of cells taken from non‐pregnant and term pregnant women. The frequency and amplitude of the oscillations were not significantly affected by OT concentrations up to 300 nM. The amplitude of the oscillations decreased in the presence of the voltage‐dependent Ca 2+ channel antagonist verapamil and gradually disappeared in Ca 2+ ‐free medium. The oscillations were further blocked by the inorganic Ca 2+ antagonist La 3+ and by the intracellular Ca 2+ ‐ATPase inhibitor 2.5‐di‐tert‐butylhydroquinone (DTBHQ). Caffeine inhibited the OT‐induced oscillations in a concentration‐dependent manner. DTBHQ and high concentrations of OT made [Ca 2+ ] i remarkably sensitive to changes in the external Ca 2+ concentration. Conclusions. The results indicate that OT‐induced [Ca 2+ ] i oscillations in human myometrial cells are due to inositol 1,4,5‐trisphosphate‐mediated release of intracellular Ca 2+ combined with capacitative as well as voltage‐dependent influx of the ion.