The aim of current trial was to investigate the SR role in the peptidoglycan elicitted alteration of myometrial contractility. For the study we used peptidoglycan from Staphylococcus aureus. In order to assess the peptidoglycan’s effect on myometrial contractility under different conditions we used the method of tensometry and took into account the average amplitude, frequency and the area under the curve of the myometrial contractions. The results of our experiments confirmed our suggestion that peptidoglycan activates myometrial contractility due to the SR depletion via IP3 receptors activation as well as the amplification of transmembrane Ca2+ influx. Under peptydoglycan the amplitude of myometrial contractions increased by nearly 7,0 ± 0.346% [n=10] compared to the control. The area under the curve increased by nearly 30,0 ± 0.256% due to both the amplitude and the duration of contractions. In our study we demonstrated that peptidoglycan makes the myometrial strip to contract even in the Ca2+-free environment throughout a few minutes. Also we demonstrated that phospholipase C blockade with U73122 doesn’t prevent entirely the stimulation of myometrial contractions by peptidoglycan. Phospholipase C blockade resulted in statistically unreliable increase in the amplitude of the peptydoglycan-stimulated myometrial contractions, their frequency decreased by 47 ± 1.05% and the area under the curve of single contraction decreased by nearly 56 ± 1.2%. But 2APB, a non selective IP3 antagonist, entirely reduced the peptidoglycan-stimulated. We suggested that peptidoglycan acts via several pathways simultaneously and Ca2+ release from SR via IP3 receptors activation is among them.