Inhibition of oxytocin-induced but not angiotensin-induced rat uterine contractions following exposure to sodium sulfide.

Low concentrations (0.15-15 microM) of sodium sulfide reversibly attenuated the contractile response of the isolated rat uterus to oxytocin without affecting angiotensin II responsiveness. These findings suggest that functionally important disulfide bonds in the rat uterine oxytocin receptor, but not the angiotensin receptor, are sensitive to hydrosulfide ion. Reduction of oxytocin receptors by hydrosulfide ion may be a mechanism by which low levels of H2S delay parturition in rats.