The Mechanism Underlying Relaxation Of Circular Myometrial Smooth Muscle Mediated By Endometrial Cells In Rat Uterus

Epithelia line ducts and tubes in many internal organs. Besides the secretion function, endometrial cells are also regulated by the neuro-transmitters, hormone and steroids. The contraction condition of smooth muscle is critical for the normal physiology statement of female reproduction system. Even though there are several papers reported that connection of epithelial cells and smooh muscle cells in tissues like airway, vessels. Few reports on the female reproduction especially in the uterus. This study, we used the rat uterus as a model to study the mechanism of cell-cell communication between endometrial cells and circular smooth muscle cells.It’s now known that the contractility of smooth muscle is tightly controlled by surrounding cells including endothelial cells and neurones. Reports about the modulation of endothelial cell and airway epithelium on the smooth muscle contractility has been noticed. Thus we hypothesized that in the rat uterus, endometrial cell may modulate the smooth muscle contraction under the stimulation of neruons. First in our experiments, contraction is increased under the stimulation of Ach in the de-endometrium tissues while partially inhibited in the intact tissues, indicated that some materials was secreted by endometrial cell under the Ach stimulation. Neither NO, released by endothelial cell under the Ach action can relax the tone of vessels, nor NaHS, a agonist of BK, have no effect on the contractility of uterus. While PGE2 can relax smooth muscle partially, and after the COX-2 antagonist indomethacin incubation, no relax was detected on the intact tissue under the stimulation of Ach. This above suggest that PGE2 secreted under the stimulation of Ach relax the uterine contraction partially.Second we study the signal pathway underlying the cell-cell crosstalk on the cell level. Ach increased Ca2+ transiently in rat endometrial cells, this effect of Ach on Ca2+ transients was blocked by the M receptors antagonist atropine and PLC inhibitor U73122, and independent of extracellular Ca2+. The membrane potential test using the voltagesensitive dye DiBCA4(3), PGE2, but not the Ach, can hyperpolarized the circular smooth muscle. This effect was inhibited by the MDL12330 A, an adenylate cyclase inhibitor, and chromanol 293 B, a blocker of cAMP-dependent K+ channels.In conclusion, our study implicated that the endometrial cell-involved regulation of smooth muscle is directed by the PGE2 secreted from endometrial cell under the stimulation of Ach. The founding unveil the connection between endometrial cells and circular myometrial cell, and light a new perspective on the female reproduction study.