Abstract

We tested the possibility that potentiation and inhibition of uterine contractions by zinc might be related to uptake or binding of zinc by uterine cells and that potentiation of contractions by ouabain might be mediated by mobilization of zinc. Zinc was accumulated by uterine muscle cells from concentrations greater than 10^-6 M. Zinc uptake was saturable with time and probably with concentration. Zinc that was normally present and most of that accumulated could not be removed by washing, even in the zinc-complexing agent, 8-hydroxyquinoline. Epinephrine, which like 8-hydroxyquinoline reversed zinc potentiation of contraction, did not detectably affect zinc contents or gain by uterine tissue. Ouabain did not affect the zinc contents of control tissues or of tissues that were accumulating zinc. Cooling to 5°C, inactivation of sulfhydryl groups with iodoacetate or the chelation of zinc in the uptake medium reduced zinc uptake. Zinc initially present or taken up was distributed in all subcellular fractions. It was concluded that free zinc ions are transported into cells independent of active transport and are sequestered there by binding to protein, possibly at —SH groups, distributed fairly uniformly throughout the myometrial cell. However, potentiation of contractility by zinc could not be correlated with zinc uptake, and it was postulated to involve zinc binding at an undetectably small number of superficial sites. Whether ouabain potentiated contractions by mobilizing this zinc could therefore not be determined. Zinc inhibition of contractility may have been related to zinc binding.