The work deals with the study of molecular and membrane mechanisms of uterotonic peptide hormone oxytocin action on Ca ions homeostasis in the uterus myocites and activity of passive and active transport systems of this cation, localized in the myometrium subcellular structures. Biochemical mechanisms of additional Ca2+ influx into the myometrium cells from extracellular environment activated by oxytocin and thapsigargin were determined. Such Ca2+ influx has got the name of capacitative cation entry (CCE), or which is activated by intracellular store depletion (store-operated calcium entry). It was shown that cells from the nonpregnant human myometrium and PHM1-41 cells (immortalized pregnant human myometrial cells) expressed endogenous hTrpC1, 3, 4, 6 and 7 mRNA. The membrane-permeable derivative of diacylglycerol (OAG) stimulated an increase in oscillations of intracellular free Ca2+ concentration in PHM1-41 and myometrium cells. OAG-induced Ca2+ -oscillations were not affected by inhibition of PKC. It was proved that hTrpC channels take part in the regulation of free Ca ions concentration in the myometrium cells. On the basis of results of experiments, conducted on myometrium plasma membrane fraction, the conclusion was made that oxytocin does not influence the passive Ca2+ efflux. It was shown that peptyde hormone partially inhibited Ca2+ accumulation in plasma membrane fraction. Oxytocin also partially inhibited endoplasmic reticulum calcium pump activity of the myometrium cells. The conceptual pattern of myometrial Ca2+ exchange regulation by oxytocin is offered.