The combined use of estrogen and progestin in oral contaceptives provides synergistic anti-ovulatory effect that directly decreases the secretion of the gonadotropin-releasing hormone (GnRH) from the hypothalamus. This negative feedback mechanism disrupts ovulation by interfering with the hypothalamus-pituitary-ovary axis and gonadotropin secretion from the pituitary. The progestin component reduces or suppresses LH release and the LH surge that is necessary for ovulation. The estrogen component reduces or suppresses the follicle-stimulating hormone (FSH) that prevents the selection and maturation of the dominant follicle. Other contributing effects include delayed maturation of the endometrium (that prevents implantation of ova) and the development of viscous cervical mucus (an effect that is considered as major mechanism of action of estrogen-progestin oral emergency contraception.