PROGESTERONE AND ESTROGEN IN THE EXPERIMENTAL CONTROL OF OVULATION TIME AND OTHER FEATURES OF THE ESTROUS CYCLE IN THE RAT
- 1 December 1948
- journal article
- research article
- Published by The Endocrine Society in Endocrinology
- Vol. 43 (6) , 389-405
- https://doi.org/10.1210/endo-43-6-389
Abstract
In normal rats with predictably regular 4-day and 5-day cycles, respectively, a series of expts. is described, whereby ovulation time and other features of the estrous cycle may be either accelerated or retarded. In the normal 5-day cycle, injn. of 1-2 mg. of progesterone on the 3d day of diestrus accelerates ovulation and vaginal cornification about 24 hrs. Equivalent results follow admn. of certain estrogens on the 2d day of diestrus. Progesterone does not accelerate the 4-day cycle when injected on the final (2d) day of diestrus. The 4-day cycle is retarded 1 day by injn. of 1.5 mg. of progesterone on the 1st day of diestrus, becoming thus a 5-day cycle. (Continued daily injn. of this dose for n days retards ovulation n days.) In such an artificial 5-day cycle, injn. of progesterone on the 3d day of diestrus, omitting treatment on the 2d day, accelerates the expected ovulation and vaginal changes about 24 hrs., just as it does in the normal 5-day cycle. Similarly, in the artificial 5-day cycle, treatment with estrogen on the 2d day of diestrus accelerates ovulation. Per-sistent-estrous rats of the defective DA strain are refractory to estrogen in the respect that ovulation and luteinization cannot be induced in them by estrogen, even when treated during the dies-trous intervals resulting from earlier progesterone treatment. However, during pseudopregnancies induced in such animals by daily injn. of progesterone (1.5 mg.), injn. of estrogen has produced ovulation in a significant number of cases. Thus progesterone "suppresses" ovulation and other features of estrus only under certain conditions. When estrogen levels are elevated, progesterone facilitates ovulation, at least in the rat. This it may accomplish by modification of the threshold of the LH-release mechanism to estrogen or perhaps by modification of estrogen metabolism.Keywords
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