Old, new and the newest concepts of inhibition of luteolysis during early pregnancy in pig.
In 1977 Bazer and Thatcher proposed that maternal recognition of pregnancy in the pig involves the secretion of PGF(2alpha) towards the uterine lumen (exocrine) rather than towards the uterine venous drainage (endocrine) as occurs in the non-pregnant pig during the mid to late stages of the estrous cycle. The retrograde transfer of PGF(2alpha) from the venous blood and uterine lymph into the uterus and the ability of the uterine vein and artery wall to accumulate PGF(2alpha) could constitute a part of putative mechanism of corpus luteum protection during early pregnancy. A luteotropic/anti-luteolytic effect of PGE(2) in the pig also has been frequently demonstrated and it seems that the most effective agent in changing PGE(2):PGF(2alpha) secretion is estradiol. The role for oxytocin during luteolysis and early pregnancy is controversial. It appears, however, that the main function of this hormone is autocrine and/or paracrine stimulation of PGF(2alpha) secretion. Pig trophoblastic interferons, unlike those of ruminants, do not themselves exert an anti-luteolytic effect in pigs. It is likely, that cytokines and angiogenic growth factors are involved in the initiation of luteolysis and/or maintenance of corpora lutea (CL).A discovery of functional LH receptors in porcine endometrium opened a new possibility for this hormone in luteolysis and perhaps in recognition of pregnancy in pigs. The endogenous LH pulses can provoke prostaglandin secretion from endometrium in pigs. On the other hand prolongation of up-regulation of LH receptors in endometrium of early pregnant gilts can additionally increase angiogenic factor production before the process of implantation is completed. Finally new integrated concepts of luteolysis and inhibition of luteolysis in pigs based on selectively reviewed information are presented.
Institute of Animal Reproduction and Food Research of Polish Academy of Sciences, Division of Reproduction Endocrinol and Pathophys, P.O. Box 55, ul. Tuwima 10, 10-747 Olsztyn, Poland. ziecik@pan.olsztyn.pl
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D000818:Animals; D003338:Corpus Luteum / Q000502:physiology*; D016207:Cytokines / Q000502:physiology; D015237:Dinoprost / Q000378:metabolism; D015232:Dinoprostone / Q000502:physiology; D005260:Female; D006133:Growth Substances / Q000502:physiology; D007372:Interferons / Q000502:physiology; D010121:Oxytocin / Q000502:physiology; D011247:Pregnancy; D013552:Swine / Q000502:physiology*; D014599:Uterus / Q000378:metabolism
D016207:Cytokines; D006133:Growth Substances; D010121:Oxytocin; D007372:Interferons; D015237:Dinoprost; D015232:Dinoprostone