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Preterm Labor and Primary Dysmenorrhea: Related Pathophysiology of Oxytocin and Vasopressin
Hiroshi Yamanakan addition to the supraoptic and para ventricular brain nuclei, the human fetus during labor and the uterine endometrium and decidua may be significant sources of oxytocin and vasopressin. Ovarian steroids influence the plasma release of oxytocin and vasopressin. Through receptors in the myometrium, the two hormones cause uterine contractions in pregnant and non-pregnant women. There has been no clear increase in the plasma concentration of oxytocin or vasopressin at the beginning of human labor, whether preterm or term; however, there may be an increase in the pulse frequency with which oxytocin is released into the bloodstream as labor progresses. Vasopressin is stronger than oxytocin on confined myometrium from ladies going through Cesarean area at term. The two receptors have about the same concentration in myometrium. There is a tendency for the density of oxytocin and vasopressin via receptors to rise at the beginning of labor, both preterm and term, but at least one of the receptors may be expressed differently in different myometrium cells. The receptors are markedly down regulated in advanced labor or after oxytocin treatment. The therapeutic effect of the oxytocin and vasopressin via receptor blocking oxytocin analogue, artosiban, in the condition is evidence of the significance of oxytocin and vasopressin in the mechanisms of preterm labor. In ladies with essential dysmenorrhea the plasma centralization of vasopressin is raised. In nonpregnant women, the in vivo effect of vasopressin on uterine activity is approximately five times greater than that of oxytocin, and it increases prior to menstruation. As a result, there is a premenstrual rise in the density of the oxytocin receptor and the density of the vasopressin via receptor. Dysmenorrhea can be treated effectively with atosiban and the non-peptide compound SR 49059, which binds to the two receptors in a manner similar to that of atosiban.