Influence of estradiol and progesterone withdrawal on the secretion of and the temporal correlation between pulses of oxytocin and prostaglandin F2(alpha) in ewes.
The primary objective was to examine the effects of estradiol and the progesterone receptor antagonist onapristone on the pulsatile secretion of prostaglandin F(2alpha) (PGF(2alpha)) and ovarian and pituitary oxytocin. A 2 x 2 factorial arrangement of estradiol and onapristone treatments was administered to groups of 5 ewes after destruction of ovarian follicles on Day 8 of the cycle. Estradiol treatments consisted of the administration of a silicone elastomer implant, either containing or not containing estradiol, on Day 8 plus 50 microg of estradiol or corn oil on Days 11 and 12. Onapristone (2 mg/kg) or its vehicle were administered on Day 13, immediately preceding the simultaneous collection of blood samples from the carotid artery, jugular vein, and vena cava at 7.5-min intervals for 7 h. Ewes were immediately killed for measurements of uterine oxytocin receptor concentrations and phosphatidylinositide turnover. More oxytocin pulses were detected in the jugular vein than in the carotid artery (p < 0.01), suggesting that the pituitary is a source of oxytocin. A similar number (p > 0.1) of PGF(2alpha) pulses were correlated with oxytocin pulses as were not. The linked PGF(2alpha) pulses were longer in duration (p = 0.01) with a tendency toward a higher amplitude (p = 0.08). The corresponding vena caval oxytocin pulses had a longer duration (p = 0.02) than those not linked to PGF(2alpha). Estradiol increased oxytocin receptor concentrations and the turnover of phosphatidylinositides (p = 0.02) without affecting PGF(2alpha) pulse characteristics. Onapristone increased (p = 0.03) PGF(2alpha) pulse amplitude. Although a lower than expected temporal correlation between oxytocin and PGF(2alpha) pulses was observed, the distinguishing characteristics of linked pulses may be indicative of their physiological significance.
Walker
D L
DL
Department of Veterinary Biosciences, College of Veterinary Medicine, University of Illinois at Urbana-Champaign, Urbana 61081, USA.
Weston
P G
PG
Hixon
J E
JE
D000818:Animals; D015237:Dinoprost / Q000378:metabolism*; D004958:Estradiol / Q000008:administration & dosage / Q000378:metabolism*; D005260:Female; D006067:Gonanes / Q000008:administration & dosage; D006727:Hormone Antagonists / Q000008:administration & dosage; D003341:Luteolysis / Q000187:drug effects / Q000502:physiology; D010121:Oxytocin / Q000378:metabolism*; D010716:Phosphatidylinositols / Q000378:metabolism; D011374:Progesterone / Q000378:metabolism*; D018045:Receptors, Oxytocin / Q000378:metabolism; D011980:Receptors, Progesterone / Q000037:antagonists & inhibitors; D012756:Sheep; D013997:Time Factors; D014599:Uterus / Q000187:drug effects / Q000378:metabolism
D006067:Gonanes; D006727:Hormone Antagonists; D010716:Phosphatidylinositols; D018045:Receptors, Oxytocin; D011980:Receptors, Progesterone; D011374:Progesterone; D004958:Estradiol; D010121:Oxytocin; D015237:Dinoprost; C053238:onapristone