Abstract
This work was undertaken to investigate some of the various factors
involved in the control of luteal activity in the sheep and goat.
Administration of ACTH immediately prior to the expected time of
luteolysis, maintained progesterone secretion, decreased the release
of PGF2x and oxytocin, and delayed oestrus. The mechanism appears to
involve a reduction in the sensitivity of the uterus to oxytocin,
via a reduction in endometrial oxytocin receptors.
To examine the significance of testosterone secretion immediately
prior to luteolysis, the steroid was administered in the mid-luteal
phase, and testosterone synthesis was also blocked with
spironolactone. While both treatments had some minor effects on
hormone release in sheep, in the goat they were significant.
Testosterone administration induced premature luteolysis with
release of PGF2 and oxytocin, whereas spironolactone inhibited
luteolysis and associated hormone release. It would appear that in
the goat, but not in the sheep, testosterone may be a significant
precursor for oestrogen synthesis.
Physiological doses of progesterone for 15 days were found to
stimulate endometrial oxytocin receptors and uterine sensitivity to
oxytocin in the goat. Oestradiol was found not to be essential for
this effect, and had no similar action, but was found to potentiate
the action of progesterone.
The release of oxytocin at various times of the ovine oestrous cycle
was pulsatile, even just after oestrus. While PGFza, a product of
the cycloxygenase pathway of arachidonic acid, has been cited as a
major stimulus to the release of luteal oxytocin in sheep, it is
possible that the lipoxygenase metabolites may also be involved.
Intra-uterine administration of nordihydroguaiaretic acid (NDGA) a
5-liрохygenase inhibitor, delayed luteolysis and this was associated
with reductions in luteal oxytocin release, luteal oxytocin content
and endometrial oxytocin receptors. Also intraluteal injection of
another 5-lipoxygenase inhibitor (BWA4C) reduced both basal and
PGFza-stimulated oxytocin release. In vitro studies showed that
arachidonic acid could stimulate release of oxytocin; addition
the reaction mixture of arachidonic acid and lipoxygenase increasea
release further. These effects were blocked by NDGA. However, it is
possible that the effect may have been due, at least in part, to а
non-physiological disruption of the cell membrane.