{"title":"The luteotrophic effects of estradiol and prolactin in the absence of LH in the hysterectomized, pseudopregnant rat.","authors":"D R Garris","doi":"10.3181/00379727-170-41419","DOIUrl":null,"url":null,"abstract":"Abstract The ability of estradiol and prolactin to substitute for LH as luteotrophins was investigated in Day 5 (Day 1 = ovulation)-hysterectomized pseudopregnant (PSP) rats. All animals received either a sc injection of oil, 1 μg estradiol (E-1), or 150 μg prolactin (PRL) on Day 9 in combination with either a normal horse serum (NHS) or LH antiserum (LHAS) injection. The ability of oil, E-1, or PRL to maintain luteal function was assessed by monitoring serum progesterone levels through Day 12 and their direct effects on the ovary monitored by measuring luteal and extra-luteal ovarian tissue concentrations of estradiol and progesterone on Day 12. NHS treatment in combination with either oil, E-1, or PRL maintained elevated serum progesterone levels through Day 12 of PSP. LHAS/oil-treated rats underwent luteolysis while E-1 and PRL effectively maintained luteal function in LHAS-treated animals. PRL raised luteal and extraluteal ovarian estradiol concentrations compared to oil/NHS-treated controls and LHAS/oil-treated rats. E-1 induced an intraluteal rise in estradiol levels in LHAS-treated rats. While luteal progesterone concentrations fell following oil/LHAS treatment, E-1 and PRL effectively counteracted this LHAS-induced fall. The results of these studies indicate that (i) E-1 and PRL can effectively replace LH as luteotrophins during PSP in the rat and (ii) that PRL and E-1 effectively maintain luteal levels of estradiol and progesterone following LH deprivation. It is suggested that E-1 and PRL may exert their luteotrophic actions by either an E-1-induced increase in PRL which, in turn, acts on the luteal cells to increase intraluteal estradiol concentrations, or by a direct effect of E on the corpus luteum to bypass the requirement for LH.","PeriodicalId":20675,"journal":{"name":"Proceedings of the Society for Experimental Biology and Medicine","volume":" ","pages":"203-8"},"PeriodicalIF":0.0000,"publicationDate":"1982-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3181/00379727-170-41419","citationCount":"4","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Proceedings of the Society for Experimental Biology and Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3181/00379727-170-41419","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 4
Abstract
Abstract The ability of estradiol and prolactin to substitute for LH as luteotrophins was investigated in Day 5 (Day 1 = ovulation)-hysterectomized pseudopregnant (PSP) rats. All animals received either a sc injection of oil, 1 μg estradiol (E-1), or 150 μg prolactin (PRL) on Day 9 in combination with either a normal horse serum (NHS) or LH antiserum (LHAS) injection. The ability of oil, E-1, or PRL to maintain luteal function was assessed by monitoring serum progesterone levels through Day 12 and their direct effects on the ovary monitored by measuring luteal and extra-luteal ovarian tissue concentrations of estradiol and progesterone on Day 12. NHS treatment in combination with either oil, E-1, or PRL maintained elevated serum progesterone levels through Day 12 of PSP. LHAS/oil-treated rats underwent luteolysis while E-1 and PRL effectively maintained luteal function in LHAS-treated animals. PRL raised luteal and extraluteal ovarian estradiol concentrations compared to oil/NHS-treated controls and LHAS/oil-treated rats. E-1 induced an intraluteal rise in estradiol levels in LHAS-treated rats. While luteal progesterone concentrations fell following oil/LHAS treatment, E-1 and PRL effectively counteracted this LHAS-induced fall. The results of these studies indicate that (i) E-1 and PRL can effectively replace LH as luteotrophins during PSP in the rat and (ii) that PRL and E-1 effectively maintain luteal levels of estradiol and progesterone following LH deprivation. It is suggested that E-1 and PRL may exert their luteotrophic actions by either an E-1-induced increase in PRL which, in turn, acts on the luteal cells to increase intraluteal estradiol concentrations, or by a direct effect of E on the corpus luteum to bypass the requirement for LH.