Biology of Reproduction, Vol 24, 496-504, Copyright © 1981 by Society for the Study of Reproduction

Plasma Levels of 13,14-Dihydro-15-keto Prostaglandin F₂ in Relation to Oviposition and Ovulation in the Domestic Hen (Gallus domesticus)

¹ Department of Physiology and Department of Obstetrics and Gynecology, St. Louis University School of Medicine, St. Louis, Missouri 63104

This study describes a specific radioimmunoassay with a sensitivity of 5-10 pg for the determination of 13,14-dihydro-15-keto prostaglandin F,₂ (PGFM) in plasma of laying hens in relation to oviposition (OP) and ovulation (OV). The biological activity of PGFM both in vivo and in vitro was also compared with that of PGF₂. In addition, evidence is presented that plasma PGFM concentrations are directly correlated (r = 0.968, P<0.0O1) to infused PGF₂ and that PGFM disappears from the circulation with a t of about 8 min. Serially sampled plasma PCFM levels rose from 267 pg/ml 1 h before midsequence OP to 1747 pg/ml at OP, and returned to lower levels (546 pg/ml) by 1 h post-OP. Hens laying the terminal egg of a sequence (C_tOP), which is not immediately followed by OV, displayed an increase in PGFM plasma levels from 347 pg/ml 1 h before OP to 1086 pg/ml at C_tOP, returning to basal values 1 h post-C_tOP. When OP was induced by arginine vasotocin (AVT, 0.2 µg, i.v.) 2-5 h before expected OP, plasma PGFM levels doubled at the time of expected spontaneous OP. No significant increase in either PGF or PGFM levels was noted in response to AVT-induced premature OP. Plasma PGFM also showed a peak at about the time of the first OV of the next sequence. Both PGFM and PGF₂ stimulate uterine contractility in vitro and promote OP in vivo, but PGFM is 3 orders of magnitude less potent than PGF₂. These results suggest that 1) PGF₂ is metabolized to PGFM, and PGFM plasma levels reflect relative changes in PGF₂ levels; 2) in the fowl, as in other species, the biological activity of PGFM is less than 1% of that of PGF₂; and 3) plasma PGFM peaks at OP are not solely the result of increased uterine activity or AVT-stimulated PG production. Rather, PG synthesis and release may represent the primary event responsible for expulsion of the egg from the shell gland.

Note:
ACKNOWLEDGMENTS We are indebted to Drs. K. Kirton and J. Pike, The Upjohn Co., for providing antiserum and reference compounds and to Dr. H. V. Biellier, University of Missouri, Columbia, for supplying the experimental animals. We also thank Miss Jan Kirchoff for the careful typing of the manuscript.

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