1993
DOI: 10.1016/0020-7292(93)90188-3
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Stimulation of vasopressin release in women with primary dysmenorrhea and after oral contraceptive treatment — Effect on uterine contractility

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Cited by 10 publications
(16 citation statements)
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“…This has been confirmed by the use of a therapeutic treatment of dysmenorrhea by oral contraceptives, which works by reducing the plasma levels of OT, VP, and estrogen receptor (ER) (8,10,16). In this case, involvement of the VPR system in giving rise to primary dysmenorrhea seems to be more important than the OTR system (20).…”
supporting
confidence: 50%
See 1 more Smart Citation
“…This has been confirmed by the use of a therapeutic treatment of dysmenorrhea by oral contraceptives, which works by reducing the plasma levels of OT, VP, and estrogen receptor (ER) (8,10,16). In this case, involvement of the VPR system in giving rise to primary dysmenorrhea seems to be more important than the OTR system (20).…”
supporting
confidence: 50%
“…Additional etiologic factors might include substances involving the coordination of myometrial contractility, such as oxytocin (OT), vasopressin (VP), and prostaglandin (PG) F 2a (7). Both VP and OT plasma levels appear to be increased in women with dysmenorrhea (8)(9)(10)(11). Oxytocin receptor (OTR) and vasopressin receptor (VPR) have been demonstrated to be present in the myometrium of nonpregnant women (12,13).…”
mentioning
confidence: 97%
“…It is open to question whether endogenous vasopressin concentrations of a thirtieth of those required to evoke slight to moderate dysmenorrhea-like pain in healthy women can indeed cause severe dysmenorrhea. Moreover, the plasma vasopressin concentrations increasing menstrual pain in women with dysmenorrhea after a bolus injection of lysin-vasopressin [26] can be calculated to have been 10 times higher (i.e., 20 pmol/l; calculations by Stefan Lundin) than that of endogenous arginine-vasopressin found by the Åkerlund team [7,25] in dysmenorrheic women.…”
Section: Discussionmentioning
confidence: 96%
“…Uterine hypercontractility and menstrual pain induced by lysine-vasopressin infusion were abolished by the vasopressin antagonist [7,23]. The plasma concentration of lysin-vasopressin during these experiments [7,23], which evoked slight to moderate dysmenorrhea-like pain in normal women, can be calculated to have been 30 times higher (i.e., 60-65 pmol/l; calculations by Stefan Lundin, Department of Clinical Pharmacology, Lund University Hospital, Lund, Sweden) than the concentration of endogenous arginine-vasopressin (2 pmol/l) found by the Åkerlund team on the 1st day of menstruation in dysmenorrheic women [7,25]. It is open to question whether endogenous vasopressin concentrations of a thirtieth of those required to evoke slight to moderate dysmenorrhea-like pain in healthy women can indeed cause severe dysmenorrhea.…”
Section: Discussionmentioning
confidence: 97%
“…Dadurch wird das Substrat für die Prostaglandin-und Leukotrienproduktion verringert.Die Verringerung der Prostaglandin-und Leukotrienkonzentration im Menstrualblut konnte in mehreren Untersuchungen gezeigt werden [5,8]. Auch eine Reduktion des intrauterinen Druckes unter OC-Gabe wurde nachgewiesen [12,13].…”
Section: Hormonale Kontrazeptivaunclassified