Factors in diminution of uteroglobin secretion in the rabbit.
Uteroglobin was measured under various hormonal conditions: pregnancy, pseudopregnancy, pseudopregnancy with exogenous progesterone, pseudopregnancy with exogenous 20alpha-hydroxyprogesterone, ovariectomy with exogenous progesterone, ovariectomy with exogenous estrogen, ovariectomy with exogenous estrogen and progesterone, and ovariectomy with either exogenous progesterone or estrogen and progesterone, plus uterine trauma. In pregnant females, uteroglobin levels diminished sharply after day 9. In pseudopregnancy, high concentrations were maintained through day 14. Although exogenous progesterone did not prevent this decrease in pseudopregnant females, re-elevation occurred in the continued presence of progesterone. A similar pattern of decline and re-elevation was found in ovariectomized females that received injections of estrogen and progesterone. With an increase in estrogen dosage, the period of uteroglobin secretion was shorter and the magnitude lower. Ovariectomized females receiving only progesterone did not manifest a clear uteroglobin diminution. Uterine trauma on day 7 of exogenous steroid administration to ovariectomized females was followed by a diminution in uteroglobin. At the dosage level used, administration of 20alpha-hydroxyprogesterone did not affect the peak uteroglobin secretion occurring on day 5 of pseudopregnancy. Ovariectomized females receiving estrogen or sesame oil vehicle had barely detectable levels of uteroglobin. A uteroglobin-estrogen complex is suggested as a possible inhibitor of uteroglobin synthesis by a feedback inhibition pathway in pseudopregnant females and in ovariectomized females treated with progesterone plus estrogen. In pregnant females, a uteroglobin-estrogen complex and/or the uterine decidual response to implantation could control uteroglobin synthesis.[1]References
- Factors in diminution of uteroglobin secretion in the rabbit. Barfield, M.A., Stambaugh, R., Mastroianni, L., Storey, B.T. Fertil. Steril. (1976) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
