Luteal peptides and intercellular communication.

The variety of peptides synthesized by the corpus luteum (relaxin, vasopressin, oxytocin and oxytocin-related neurophysin) and their possible intracellular effects are reviewed. After luteinization of the granulosa cells and in response to LH and FSH, the output of oxytocin is increased. In addition, insulin-like growth factor is a very potent stimulus of oxytocin secretion. Although luteal cells respond to gonadotrophins by increased production of progesterone, there is no further secretion of oxytocin. Oxytocin is localized in large luteal cells which seem not to be under the direct control of gonadotrophins. Synthesis of luteal oxytocin seems to occur during the early luteal phase according to measurements of oxytocin mRNA. Highest tissue concentrations and secretion under in-vitro conditions were observed during the mid-luteal phase, and so synthesis, storage and secretion are unlikely to occur concomitantly. Under in-vitro conditions, oxytocin is secreted concomitantly with neurophysin and progesterone, and there appears to be some form of communication between small and large luteal cells for the secretion of progesterone and oxytocin under in-vivo conditions. Evidence has been obtained that oxytocin may have local effects in the ovary by inhibition of secretion (synthesis ?) of progesterone, especially during the early luteal phase. A mechanism can be suggested whereby, under physiological conditions, oxytocin may delay the increase of progesterone by inhibition of progesterone secretion and therefore delay down regulation of its own receptor. This would prolong the life-span of the CL and the oestrous cycle. Exogenous progesterone given on Days 1-4 shortens the cycle to about 12 days. The best evidence that oxytocin may be involved in controlling luteolysis comes from immunization experiments in ewes and goats, but there is no clear evidence of this type for cattle. Basal concentrations of oxytocin at the end of the luteal phase may interact with oxytocin receptors after the inhibitory effect of progesterone in the uterus is reduced, thus initiating synthesis of PGF-2 alpha.