Oxytocin and the timing of parturition. Influence of oxytocin receptor gene expression, oxytocin secretion, and oxytocin-induced prostaglandin F2 alpha and E2 release.
Oxytocin receptor (OTR) gene expression was studied in various tissues of the reproductive tract of pregnant cows and compared with ligand binding activity. Myometrium, intercaruncular endometrium, caruncular endometrium, cotyledons and fetal membranes, as well as the uterine cervix of pregnant cows expressed the bovine OTR gene. Receptor concentrations, measured by ligand binding to crude microsomal pellets, were comparable to OTR mRNA signal strength in all instances indicating that the receptor protein formation is probably regulated at the transcriptional level. During bovine pregnancy OTR gene expression was initiated at different times depending on the tissue. The expression of the gene for OT peptide was not found in any of the bovine uterine tissues but was found in the corpora lutea at term and during parturition and then at relatively low levels. Therefore endogenous OT is derived almost exclusively from the pituitary during bovine pregnancy. OT secretion occurred in a pulsatile manner during pregnancy; a significant increase in pulse amplitude was observed during the last days before delivery and a large surge was associated with active labor and delivery. We postulate that the temporal order of OTR gene expression in the uterine and intrauterine tissues is a factor in the synchronization of the events that eventually lead to the onset of parturition. Because OT receptor mediates different actions in different tissues OT has multiple functions in the mechanism of parturition. The peptide initiates and maintains myometrial contractions, it stimulates release of PGF2 alpha from the endometrium and fetal membranes and, as demonstrated in this study, OT induces PGE2 release from cervical tissues in an OTR dependent manner. We conclude that in pregnant cows, OT participates both in the events that prepare the reproductive tract for birth and initiate the birth process.
Fuchs
A R
AR
Institute for Hormone and Fertility Research, Hamburg, Germany.
Fields
M J
MJ
Freidman
S
S
Shemesh
M
M
Ivell
R
R
D000818:Animals; D002417:Cattle; D002584:Cervix Uteri / Q000378:metabolism; D015237:Dinoprost / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004717:Endometrium / Q000378:metabolism; D005321:Extraembryonic Membranes / Q000378:metabolism; D005260:Female; D015870:Gene Expression; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D007743:Labor, Obstetric / Q000502:physiology*; D008024:Ligands; D009215:Myometrium / Q000378:metabolism; D010121:Oxytocin / Q000235:genetics / Q000494:pharmacology / Q000502:physiology*; D010920:Placenta / Q000378:metabolism; D011247:Pregnancy; D012333:RNA, Messenger / Q000235:genetics / Q000378:metabolism; D018045:Receptors, Oxytocin / Q000235:genetics* / Q000378:metabolism; D013997:Time Factors
D008024:Ligands; D012333:RNA, Messenger; D018045:Receptors, Oxytocin; D010121:Oxytocin; D015237:Dinoprost; D015232:Dinoprostone