Prolactin and the Luteotropic Complex in Hamsters

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Abstract
Inquiry has been made concerning the effectiveness of prolactin as a luteotropin in hypophysectiomized and in pituitary-intact female hamsters. The corpora lutea (CL) of the cycle typically become ischemic by the onset of the ensuing estrus. Those of pseudopregnancy are typically ischemic prior to the end of Day 8 of pseudopregnancy. CL of cyclic females hypophysectiomized on Day 2 became ischemic 2 days later. Those of pseudopregnant females hypophysectomized on Day 1 or 2 of pseudopregnancy became ischemic 2-4 days later. Thus, a continuing pituitary stimulus is essential for sustained function of the CL of pseudopregnancy. One to 3 pituitary implants from male donors did not delay ischemia in hypophysectomized cyclic females nor did 1 or 2 implants delay ischemia in hypophysectomized pseudopregnant females. However, 2 or 3 pituitary implants in cyclic females with intact pituitaries evoked a pseudopregnancy of approximately normal duration. Thereafter, a series of spontaneous pseudopregnancies recurred. Ovine prolactin administered to cyclic females likewise evoked a pseudopregnancy of normal duration. Five females receiving porcine FSH [follicle-stimulating hormone] displayed a normal 4-day cycle, confirming other studies. Equine LH hastened the onset of ischemia of CL of the cycle in 6 of 10 females. In 2 females heat was delayed 12 hr. It is concluded that prolactin plus at least one presently unidentified synergist of pituitary origin, or produced under the influence of an intact pituitary, constitutes a luteotropic complex in golden hamsters. Cyclic females hypophysectomized on Day 2 or 3 and thereafter administered ovine prolactin exhibited hyperemic CL beyond the date of the next anticipated estrus, remaining hyperemic up to 6 days beyond the usual time of involution of CL of the cycle, but not beyond the term of normal pseudopregnancy. It is inferred that the prolactin preparation contained the synergist as a contaminant. Prolactin injections in pseudopregnant females with intact pituitaries did not prolong pseudopregnancy, the CL becoming ischemic on schedule. Neither did 1-3 pituitary implants in hysterectomized females prolong the functional life of the CL beyond the normal 14-16 days. It is plausible that a fluctuation in the release of the synergist by an intact pituitary under direct hypothalamic regulation may be the cause of regression of the CL of pseudopregnant and pseudopregnant-hysterectomized females.

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