Prostaglandins in the ovary and fallopian tube.
More than 20 years following the recognition of a possible role for eicosanoids in ovarian function a physiological role for prostaglandins and/or leukotrienes in human ovulation, corpus luteum function and tubal motility remains to be demonstrated. With respect to ovarian function, the well-characterized preovulatory rise in eicosanoid production in animal species and humans, in conjunction with the large body of experimental evidence employing inhibitors of prostaglandin synthesis and replacement of individual prostaglandins, has provided strong evidence for a role in follicular rupture independent of other LH-mediated ovulatory events. The possible mechanism of prostaglandin-induced follicle rupture may involve stimulation of proteolytic activity via substances such as plasmin and PA; however, this is controversial. A role for prostaglandins in ovarian luteal function is well established in laboratory animals and large ruminant species, where PGF2 alpha derived from the uterus has been demonstrated to be the luteolytic factor. In humans, luteal function may be influenced by local intraovarian eicosanoid production, which has been suggested to involve the paracrine interaction of local ovarian hormones such as oxytocin, noradrenaline, insulin and IGFs, to name but a few. Several lines of evidence have also implicated prostaglandins as an aetiological factor in ovarian pathological states such as seen in the OHSS. However, the bulk of clinical experimental evidence to date has failed to support this contention. Prostaglandin production has likewise been well characterized in the fallopian tube in both humans and animal species. Whereas a role for prostaglandins in tubal transport has been demonstrated with animal species such as the rabbit, several studies have failed to define a similar function in humans. More recently, direct injections of prostaglandin analogues into the fallopian tube and the corpus luteum have been shown to be efficacious as a treatment for ectopic pregnancy. Whether the primary mechanism of action involves effects on tubal musculature or corpus luteum function, or is simply a local vascular effect, remains to be demonstrated. Therefore, although the physiological role for eicosanoids in ovarian and tubal function remains unclear, particularly in the human, an increasing body of recent evidence has suggested an important paracrine function for this class of cellular mediators whose interaction with other more recently characterized local ovarian factors has only begun to be recognized.
Gelety
T J
TJ
Department of Obstetrics and Gynaecology, UCLA School of Medicine 90025.
Chaudhuri
G
G
D000818:Animals; D003338:Corpus Luteum / Q000502:physiology; D015237:Dinoprost / Q000502:physiology; D015232:Dinoprostone / Q000502:physiology; D011464:Epoprostenol / Q000502:physiology; D005187:Fallopian Tubes / Q000737:chemistry* / Q000502:physiology; D005260:Female; D006801:Humans; D015289:Leukotrienes / Q000502:physiology; D006080:Ovarian Follicle / Q000502:physiology; D016471:Ovarian Hyperstimulation Syndrome / Q000503:physiopathology; D010053:Ovary / Q000737:chemistry* / Q000502:physiology; D010060:Ovulation / Q000502:physiology; D011247:Pregnancy; D011271:Pregnancy, Ectopic / Q000628:therapy; D011453:Prostaglandins / Q000378:metabolism / Q000502:physiology* / Q000627:therapeutic use
D015289:Leukotrienes; D011453:Prostaglandins; D015237:Dinoprost; D011464:Epoprostenol; D015232:Dinoprostone