The Life Cycle of the Corpus Luteum by Rina Meidan

Author:Rina Meidan
Language: eng
Format: epub
Publisher: Springer International Publishing, Cham

8.6 Hypophyseal Hormones

Both PRL and LH are luteotropic within the canine CL. There is, however, controversy concerning the exact timing and the extent to which both factors are required for luteal maintenance in the dog [51–55].

Thus, during the first 2–4 weeks of its development, the canine CL appears to be at least in part refractory to hypophyseal influence as early hypophysectomy (on day 4 after ovulation) resulted in only temporary suppression of P4 secretion, which was attributed to postoperative stress. This was followed by a 6 to 10-day recovery phase, with the luteal lifespan, however, being shortened compared with controls [55]. In the same study, when dogs were hypophysectomized on day 18 after ovulation, the suppression of CL function was permanent. Based on these observations, it has been concluded that in the dog luteal function is autonomous during a certain period, at least regarding hypophyseal support, or in a broader sense, gonadotropic support. Taking into account the length of the recovery phase observed after early hypophysectomies, it has been postulated that the refractory phase ends on about day 24–28 after ovulation [55]. A contradiction exists, however, with results in a study by Concannon [52], in which hypophysectomies performed between days 10 and 50 of the luteal phase always resulted in premature cessation of CL function within 3–17 days, supporting the conclusion that canine CL is chronically dependent upon gonadotropic support. Further studies are needed to clarify these discrepancies.

Nevertheless, during the second half of diestrus, hypophyseal hormones are needed for maintaining canine CL function, with PRL being the predominant luteotropic factor. The latter is absolutely required from day 25 of the luteal lifespan onward, as clearly presented in functional studies utilizing the dopamine agonist, bromocriptine, for suppression of PRL secretion [53]. Interestingly PRL, but not LH, was able to reverse the negative effects of bromocriptine on P4 production [56]; this further supports the afore-presented, postulated time-dependent luteal sensitivity to hypophyseal support. Suppression of LH function at comparable time points or later during the luteal lifespan (i.e., on days 25, 30, 31 of the luteal phase [53], or day 42 after the onset of estrus [51], or between days 30–34 and at day 40 after the LH surge [54]), resulted either in temporarily decreased P4 release , or did not affect circulating P4 levels, indicating the subordinate role of LH as a luteotropic agent compared with PRL. Its role, however, in regulating canine CL function is illustrated by the stimulatory effects evoked by LH treatment on PRL secretion and its direct positive effects on P4 production observed in some studies [52, 54]. PRL, on the other hand, did not stimulate LH secretion and neither did it directly stimulate P4 levels, indicating its role in maintenance or support of CL function and slowing down of luteal regression, rather than active stimulation of P4 secretion [56]. This finding is supported by the observation that the progressive luteal regression that takes place during the second half of diestrus cannot be prevented despite the increasing bioavailability of PRL and LH [57–61].

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