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PubMed2005

Effects of progesterone and estrogen on endothelial dysfunction in porcine coronary arteries.

BACKGROUND: The effects of hormone replacement therapy (HRT) on the vascular endothelium have been controversial. In this study, we determined the effects of HRT on endothelium-dependent relaxation in a porcine coronary artery model. METHODS: Coronary artery rings harvested from female swine were incubated as controls or with estrogen (10(-9), 10(-8), 10(-7) g/L), progesterone (1 x 10(-6), 1 x 10(-5), 5 x 10(-5) g/L), or a combination of the two (10(-8)g/L estrogen, 1 x 10(-5)g/L progesterone). After 24 h in tissue culture, the rings were tested on a myograph system to measure contraction and endothelium-dependent relaxation. Myograph analysis was performed with the thromboxane A2 analogue U46619 for contraction and bradykinin or sodium nitroprusside for relaxation. Nitric oxide synthase (eNOS) levels were determined by immunohistochemistry. Levels of superoxide anion in the progesterone or estrogen treated tissues were assessed by lucigenin-enhanced chemiluminescence analysis. RESULTS: In response to 10(-7)M bradykinin, porcine coronary artery rings treated with 1 x 10(-6), 1 x 10(-5) and 5 x 10(-5) g/L of progesterone showed a significant reduction in endothelium-dependent vasorelaxation by 36%, 45%, and 68%, respectively, as compared to controls (P <0.05). However, rings treated with estrogen showed no significant difference as compared to controls. Furthermore, estrogen treatment with progesterone reversed the effect of progesterone, showing no difference in vessel relaxation as compared to controls. There were no differences in endothelium-independent vasorelaxation (sodium nitroprusside) or in smooth muscle contractility (U46619) between the control and the hormone-treated groups. The eNOS immunoreactivity was reduced in progesterone-treated coronary artery rings. Furthermore, coronary endothelium exposed to progesterone showed a 59% increase in superoxide anion production, while estrogen produced a 67% decrease when compared to controls (P <0.05 for both). CONCLUSION: This data suggests that the progesterone component of HRT has a detrimental influence on endothelium-dependent relaxation. This effect appears to be related to decreased eNOS levels, as well as increased consumption of NO by superoxide anion in the endothelium of tissues exposed to progesterone. Estrogen can block progesterone-induced endothelial dysfunction and superoxide anion production in the pig coronary artery model.

Animals↗
PubMed2005

The steroid-binding subunit of the Na/K-ATPase as a progesterone receptor on the amphibian oocyte plasma membrane.

Progesterone acts at a plasma membrane receptor on the Rana oocyte to initiate meiosis. A cascade of lipid messengers occurs within seconds, followed by sequential changes in membrane phospholipid composition. We now show that progesterone binding to the plasma membrane increases continuously over the first 4 h. Subsequently, about 60% of the total plasma membrane and > 90% of membrane-bound progesterone, ouabain binding sites, and Na/K-ATPase activity are internalized. Until the completion of membrane internalization, oocytes must be continuously exposed to nanomolar concentrations of exogenous progesterone for meiosis to continue. The membrane-bound progesterone remains unchanged, whereas microinjected [(3)H]progesterone is rapidly metabolized. We find that progesterone and the plant steroid ouabain compete for one of two ouabain binding sites on the oocyte surface. Ouabain blocks progesterone action and inhibits subsequent meiosis if added at any time during the first 4-5 h. Western blots of SDS/PAGE extracts of isolated oocyte plasma membranes contain a -110 kDa band which binds an antibody to the steroid-binding c-terminal domain in rat and human PR. The number of binding sites and K(d) for progesterone binding to the plasma membrane is comparable to those for low-affinity ouabain binding to the alpha-subunit of the Na/K-ATPase (112 kDa). Our results suggest that progesterone binding to the ouabain binding site on the N-terminal region of the alpha-subunit of Na/K-ATPase may modulate early plasma membrane events over the first 4-6 h. Progesterone may thus act in part through the plasma membrane Na/K-ATPase signaling system.

Animals↗
PubMed2001

Progesterone receptor isoform A inhibits isoform B-mediated transactivation in human amnion.

Human amnion cells were transfected with progesterone receptor A and/or B, and the progesterone-dependent reporter construct, mouse mammary tumor virus promoter (MMTV), linked to a luciferase gene. In progesterone receptor B-expressing amnion that had been cultured before the onset of labour, treatment with progesterone resulted in an eightfold increase of the reporter activity, whereas in laboured cells, no such increase was seen. In contrast, progesterone receptor A was a weak activator of transcription in laboured and non-laboured amniocytes. When the isoforms A and B of the progesterone receptor were co-transfected, progesterone receptor A exhibited a marked inhibitory effect on progesterone receptor B-mediated transcription. These results show that progesterone receptors A and B function differentially, and progesterone receptor A is a transdominant repressor of progesterone receptor B-mediated transcription in human term amnion.

Amnion↗
PubMed1998

Experience with a novel vaginal progesterone preparation in a donor oocyte program.

OBJECTIVE: To compare the efficacy of a vaginal progesterone preparation with our standard IM preparation within a donor egg program. DESIGN: Prospective randomized trial. SETTING: Donor egg program at a university assisted reproductive therapy program (Jones Institute for Women's Health). PATIENT(S): Couples accepted into the donor egg program because of either premature ovarian failure or evidence of diminished ovarian reserve. INTERVENTION(S): Women were randomized into either a group receiving IM progesterone replacement or a group receiving vaginal progesterone replacement. Both groups underwent Estraderm patch/progesterone treatment in a mock cycle leading to an endometrial biopsy on day 26 followed by a second cycle in which ET was performed. Subjects with residual ovarian function received a GnRH agonist. In the IM treatment group, 100 mg was administered from cycle days 15 to 27. In the vaginal treatment group, Crinone 8%, a polycarbophil-based gel preparation containing 90 mg of micronized progesterone, was administered twice daily from the evening of day 14. MAIN OUTCOME MEASURE(S): Endometrial histology, serum levels of progesterone (on days 13, 17, 20, 24, and 26), the occurrence of pregnancy, implantation rate, and pregnancy outcome. RESULT(S): Fifty-four women randomized into the vaginal progesterone treatment group and 18 women in the IM treatment group achieved ET. Mean serum progesterone levels were higher in the IM treatment group than in the Crinone group. Endometrial histology was "in phase" for all subjects in both groups. Clinical pregnancies were observed in 26 of 54 women and 5 of 18 women in the Crinone and IM progesterone groups, respectively. The ongoing pregnancy rate (PR) of 31% (17/54) and implantation rate of 23% in the subjects receiving Crinone was not statistically different from the IM progesterone group's ongoing PR of 22% (4/18) and implantation rate of 18%. CONCLUSION: Vaginal progesterone replacement with the polycarbophil gel preparation was as effective as IM progesterone in producing clinical and ongoing pregnancies within our donor egg program in the dosages administered.

17-alpha-Hydroxyprogesterone↗
PubMed1999

Oral versus intramuscular progesterone for in vitro fertilization: a prospective randomized study.

OBJECTIVE: To evaluate the efficacy of oral micronized progesterone compared with IM progesterone in oil for luteal support in patients undergoing IVF who are treated with a GnRH agonist. DESIGN: Randomized prospective clinical trial. SETTING: University-based IVF center. PATIENT(S): Women <40 years of age who were undergoing IVF with luteal GnRH pituitary down-regulation. INTERVENTION(S): Patients were randomized to receive either oral micronized progesterone (200 mg three times daily) or IM progesterone (50 mg daily). MAIN OUTCOME MEASURE(S): Progesterone levels at standardized days 21 and 28, and pregnancy and embryo implantation rates. RESULT(S): Day 21 progesterone levels were 77.6+/-13.2 ng/mL in the IM group and 81.5+/-16.2 ng/mL in the oral group. Day 28 progesterone levels were 76.3+/-15.0 ng/mL in the IM group and 53.6+/-10.1 ng/mL in the oral group. The clinical pregnancy rates were 57.9% and 45.8% for the IM and oral groups, respectively. The implantation rate per embryo was significantly higher in the IM group (40.9%) than in the oral group (18.1%). CONCLUSION(S): When used according to our protocols, oral progesterone and IM progesterone result in comparable levels of circulating progesterone. However, oral progesterone results in a reduced implantation rate per embryo.

Administration, Oral↗
PubMed1997

Acute effects of progesterone on glucose metabolism in rat adipocytes: are they modulated by endogenous adenosine?

Progesterone rapidly inhibits glucose oxidation of isolated rat adipocytes. Because this inhibition is triggered by endogenous adenosine, the present study was designed to examine the effect of the steroid on cyclic adenosine monophosphate (cAMP) accumulation, its relation to lipolysis, and the possible participation of adenosine. The results strongly indicate that physiological concentrations of progesterone increase the release of adenosine by isolated adipocytes, with maximal release at the end of a 20-minute incubation. Progesterone decreased both cAMP levels and lipolysis in quiescent adipocytes or in adipocytes stimulated by isoproterenol. The increase of endogenous adenosine may explain the decline of cAMP and glycerol levels observed with progesterone. The effects of the steroid on lipolysis disappeared when adenosine was hydrolyzed by adenosine deaminase (ADA). On the other hand, in the absence of endogenous adenosine, the effect of progesterone on the cAMP level was decreased only in isoproterenol-stimulated cells. The inhibitory effects of progesterone on cAMP and glycerol production seem not to be related directly to the adenosine A1 receptor, for selective A1 receptor antagonists (8-cyclopentyl-1,3-dipropylxanthine [DPCPX] and CP 68,247) did not counteract these effects. However, mechanisms mediated by guanyl nucleotide binding proteins cannot be excluded. The decrease of cAMP and of lipolysis may be related to a stimulation of phosphodiesterases (PDEs). When PDEs I [Ca(2+)-calmodulin-regulated PDE family) were blocked by a selective inhibitor (CP 41,757), the progesterone inhibitory effect persisted, suggesting that PDEs I are not regulated by the steroid. On the other hand, the progesterone effect on cAMP accumulation but not on lipolysis disappeared in the presence of a selective inhibitor of the PDE IV family (cAMP-dependent-specific family). Ro 20.1724. When the specific inhibitor of PDE I or PDE IV was combined with ADA, the progesterone effect on cAMP disappeared. Taken together, these results suggest that the progesterone inhibitory action on cAMP levels was not mediated through A1 receptors or through activation of PDE I, but may be related to PDE IV activities. The progesterone effect on lipolysis seemed not to be directly related to changes in cAMP levels; an effect on PDE III activities in relation with the increase of adenosine release cannot be excluded.

1-Methyl-3-isobutylxanthine↗
PubMed2000

Direct transport of progesterone from vagina to uterus.

OBJECTIVE: To compare progesterone concentrations in serum and endometrial tissue from hysterectomy specimens after vaginal or intramuscular (IM) administration of progesterone gel. METHODS: This was a randomized open study of 14 post-menopausal women undergoing transabdominal hysterectomies. Participants received either vaginal progesterone gel, 90 mg, or IM progesterone, 50 mg, at 8:00 AM and 8:00 PM on the day before surgery and at 6:00 AM on the day of surgery. Venous blood samples for progesterone measurement were collected at 8:00 AM on the day before surgery (baseline) and during surgery. After removal of the uterus, the endometrium was sampled from the anterior and posterior walls. Results were expressed as ratios of endometrial to serum progesterone concentrations x 100. RESULTS: Ratios of endometrial to serum progesterone concentrations were markedly higher in women who received vaginal progesterone (14.1 median, 8.5-59.4 range; 95% confidence interval [CI] 9.89, 38.79) compared with IM injections (1.2 median, 0.5-13.1 range; 95% CI -0.48, 7.39) (P < .005). CONCLUSION: Ratios of endometrial to serum progesterone concentrations were higher after vaginal administration of progesterone than after IM injections. Our findings in endometrial tissue specimens from hysterectomies excluded the possibility of contamination by progesterone that remained in the vagina.

Administration, Intravaginal↗
PubMedDate not supplied

Progesterone treatment during the early follicular phase of the menstrual cycle: effects on smoking behavior in women.

The goals of this study were (1) to examine the feasibility of administering progesterone to women during the early follicular phase when the endogenous estradiol and progesterone levels are low, and (2) to investigate the effects of oral progesterone treatment on smoking behavior in female smokers. Twelve subjects had two experimental sessions, within 3-9 days after the beginning of their menses. In each experimental session, subjects received a single 200-mg dose of progesterone or placebo, orally. Two and a half hours after the medication treatment, subjects were assessed for subjective response to two puffs of a cigarette and then started the self-administration period in which they had the option to exchange their token for two puffs of cigarette, 15 min apart. Subjects had low levels of estradiol and progesterone before the first and second sessions. Plasma progesterone levels peaked in 2 h following progesterone treatment. Progesterone treatment attenuated the craving for and subjective effects from smoking. Under progesterone treatment, there was a trend for decreased smoking behavior. These preliminary results suggest that the early follicular phase of the menstrual cycle may be a useful interval to investigate the effects of exogenous progesterone in female smokers. The effects of progesterone on nicotine dependence need to be studied further.

Adult↗
PubMed2001

Progesterone inhibits transcriptional activation of human chorionic gonadotropin-alpha gene through protein kinase A pathway in trophoblast cells.

The purpose of this study was to analyze the mechanism of transcriptional inhibition of human chorionic gonadotropin-alpha (hCGalpha) gene by progesterone in trophoblast cells. We stably transfected -290 bp hCGalpha promoter-CAT constructs (-290halphaCAT) into Rcho-1 cells and monitored the promoter activities. Differentiation-dependent activation of -290 bp hCGalpha promoter containing a tandem repeat of cAMP response element (CRE) was inhibited by progesterone in a dose-dependent manner. To further analyze the mechanism of the progesterone action, Rcho-1 cells stably transfected with -290halphaCAT were treated with forskolin in the presence of progesterone. Progesterone inhibited forskolin-induced transcriptional activation of hCGalpha gene. Moreover, progesterone inhibited forskolin-induced transcriptional activation of CRE-CRE-tk-CAT. These results suggest that progesterone may inhibit cAMP-induced transcriptional activation of hCGalpha gene through CRE. Although progesterone did not alter the amount of CRE-binding protein (CREB), which is a main transcriptional factor bound to CRE(s) on hCGalpha promoter, progesterone abolished forskolin-induced CREB phosphorylation. In addition, pretreatment with progesterone abolished forskolin-induced activation of nuclear protein kinase A (PKA). In conclusion, progesterone inhibits hCGalpha gene transcription, at least in part, via the CRE region by inhibiting CREB phosphorylation through PKA pathway in trophoblast cells.

Blotting, Western↗
PubMed1999

Bcl-2, survivin and variant CD44 v7-v10 are downregulated and p53 is upregulated in breast cancer cells by progesterone: inhibition of cell growth and induction of apoptosis.

Progesterone inhibits the proliferation of normal breast epithelial cells in vivo, as well as breast cancer cells in vitro. But the biologic mechanism of this inhibition remains to be determined. We explored the possibility that an antiproliferative activity of progesterone in breast cancer cell lines is due to its ability to induce apoptosis. Since p53, bcl-2 and survivin genetically control the apoptotic process, we investigated whether or not these genes could be involved in the progesterone-induced apoptosis. We found a maximal 90% inhibition of cell proliferation with T47-D breast cancer cells after exposure to 10 microM progesterone for 72 h. Control progesterone receptor negative MDA-231 cancer cells were unresponsive to 10 microM progesterone. The earliest sign of apoptosis is translocation of phosphatidylserine from the inner to the outer leaflet of the plasma membrane and can be monitored by the calcium-dependent binding of annexin V in conjunction with flow cytometry. After 24 h of exposure to 10 microM progesterone, cytofluorometric analysis of T47-D breast cancer cells indicated 43% were annexin V-positive and had undergone apoptosis and no cells showed signs of cellular necrosis (propidium iodide negative). After 72 h of exposure to 10 microM progesterone, 48% of the cells had undergone apoptosis and 40% were annexin V positive/propidium iodide positive indicating signs of necrosis. Control untreated cancer cells did not undergo apoptosis. Evidence proving apoptosis was also demonstrated by fragmentation of nuclear DNA into multiples of oligonucleosomal fragments. After 24 h of exposure of T47-D cells to either 1 or 10 microM progesterone, we observed a marked down-regulation of protooncogene bcl-2 protein and mRNA levels. mRNA levels of survivin and the metastatic variant CD44 v7-v10 were also downregulated. Progesterone increased p53 mRNA levels. These results demonstrate that progesterone at relative high physiological concentrations, but comparable to those seen in plasma during the third trimester of human pregnancy, exhibited a strong antiproliferative effect on breast cancer cells and induced apoptosis.

Annexin A5↗
PubMed1996

Progesterone inhibits cholesterol biosynthesis in cultured cells. Accumulation of cholesterol precursors.

Cells acquire cholesterol through endogenous synthesis and through receptor-mediated uptake of cholesterol-rich low density lipoprotein (LDL). Esterification of LDL-derived cholesterol is catalyzed by acyl-CoA:cholesterol acyltransferase (ACAT) in the endoplasmic reticulum (ER). Progesterone inhibits esterification, and, although the mechanism of inhibition is not completely understood, this inhibition results from progesterone's ability to inhibit the activity of multiple drug resistance (MDR) P-glycoproteins (P. DeBry and J. E. Metherall, submitted for publication). In the current manuscript, we demonstrate that progesterone inhibits cholesterol biosynthesis resulting in the accumulation of a number of sterol precursors. In Chinese hamster ovary (CHO) cells, high concentrations (100 microM) of progesterone completely blocked cholesterol production, resulting in the accumulation of lanosterol and a lanosterol precursor. Lower concentrations (40 microM) of progesterone cause plasma membrane accumulation of several sterol products. The majority of these sterols are precursors of cholesterol since they were efficiently converted to cholesterol upon removal of progesterone from the culture medium. Although very high concentrations (> 200 microM) of progesterone killed CHO cells, their growth was restored by the addition of cholesterol to the growth medium, indicating that progesterone toxicity resulted from cholesterol auxotrophy. The effect of progesterone was not unique to CHO cells; progesterone also inhibited cholesterol biosynthesis in all human cell lines tested. These observations suggest that a common progesterone-sensitive pathway is involved in both cholesterol biosynthesis and the processing of LDL-derived cholesterol.

Animals↗
PubMed1999

Progesterone regulates proliferation of endothelial cells.

The use of steroid hormones in postmenopausal replacement therapy has been associated with prevention of cardiovascular disease. Although the contribution of estradiol to endothelial cell function has been addressed, little information is available on the effect of progestins on this cell type. Here, we provide direct evidence for the presence of functional nuclear progesterone receptor in endothelial cells and demonstrate that physiological levels of progesterone inhibit proliferation through a nuclear receptor-mediated mechanism. The effects of progesterone were blocked by pretreatment with a progesterone receptor antagonist, and progesterone receptor-deficient endothelial cells failed to respond to the hormone. We evaluated the effect of progesterone by analysis of aorta re-endothelialization experiments in wild-type and progesterone receptor knockout mice. The rate of re-endothelialization was significantly decreased in wild-type mice when in the presence of progesterone, whereas there was no difference between control and progesterone-treated progesterone receptor knockout mice. FACS analysis showed that progestins arrest endothelial cell cycle in G1. The lag in cell cycle progression involved reduction in cyclin-dependent kinase activity, as shown by down-regulation in retinoblastoma protein phosphorylation. In addition, treatment of endothelial cells with progestins altered the expression of cyclin E and A in accordance with G1 arrest. These results have important implications to our current knowledge of the effect of steroids on endothelial cell function and to the overall contribution of progesterone to vascular repair.

Animals↗
PubMed2000

Biodegradable progesterone microsphere delivery system for osteoporosis therapy.

The purpose of this study was to formulate and characterize a controlled-release biodegradable delivery system of progesterone for the treatment or prevention of osteoporosis. Microspheres of progesterone were formulated using copolymers of poly(glycolic acid-co-dl-lactic acid) (PGLA 50/50 and PGLA 15/85) and poly(L-lactic acid) (L-PLA) of similar molecular weight by the emulsion solvent evaporation technique. The effects of process variables, such as volume fraction, polyvinyl alcohol (PVA) concentration, polymer composition, and stir speed during preparation, on the yield, encapsulation efficiency (EEF), particle size distribution, in vitro release profiles of progesterone, and surface morphology of progesterone microspheres were investigated. Increasing the volume fraction from 9% to 22% increased the EEF without significantly increasing the yield; however, the rate of progesterone release from the microspheres decreased. Increasing the PVA concentration from 1% to 5% had no significant influence on the EEF, but the rate of progesterone release from microspheres increased. Polymer composition had no significant effect on the EEF, but had a significant effect on the particle size distribution, surface morphology, and release rate of progesterone from the microspheres. Stir speed did not have a significant influence on the EEF; however, stir speed influenced particle size distribution and the rate of progesterone release from microspheres of the same sieve-size range. The results suggest that controlled release of progesterone is possible by varying the different process variables, and that PGLA 50/50 provided the slowest release of progesterone. This should provide a means of delivering progesterone for months for the treatment or prevention of osteoporosis in postmenopausal women.

Antimicrobial Cationic Peptides↗
PubMed1993

Immunolocalization of oestrogen and progesterone receptors in the human decidua in relation to prolactin production.

The distribution of oestrogen and progesterone receptors within the decidualized stroma of the uterus was examined in early and term human pregnancy and the results related to the effect of oestradiol and progesterone on prolactin production by decidua in vitro. In early pregnancy progesterone receptors were present in the nucleus of decidualized cells of both the capsularis and parietalis but not in glandular cells. In contrast at term progesterone receptors were located within the cytoplasm of decidual cells. Oestrogen receptors were detected only in the nucleus and were present in greater amounts in decidua capsularis than parietalis in early pregnancy, but were not detectable in term decidua. Both oestrogen and progesterone receptors were present in the nuclei of cells of arterioles within the decidua. In early pregnancy prolactin production decreased during in-vitro culture of decidua parietalis but was maintained in decidua capsularis, associated with an increase in progesterone production by the decidua capsularis. In term decidua, prolactin production in vitro was only stimulated by a combination of oestradiol and progesterone. These results suggest, firstly, that maintained decidualization and prolactin production by decidua capsularis during treatment of women in early pregnancy with the anti-progestin mifepristone is not due to an absence of progesterone receptor; secondly, there is a shift in immunoreactive progesterone receptor in decidual cells from the nucleus in early pregnancy to the cytoplasm in term pregnancy. This may indicate an alteration in the action of progesterone around the time of parturition; and thirdly, in term decidua, progesterone, apparently acting through the cytoplasmic receptor, is active in increasing prolactin production in vitro only when combined with oestradiol.

Cells, Cultured↗
PubMed2003

Different effects of subnormal levels of progesterone on the pulsatile and surge mode secretion of luteinizing hormone in ovariectomized goats.

This study tested the hypothesis that endocrinological threshold levels of progesterone that induce negative feedback effects on the pulsatile and surge modes of LH secretion are different. Our approach was to examine the effects of subnormal progesterone concentrations on LH secretion. Long-term ovariectomized Shiba goats that had received implants of silastic capsules containing estradiol were divided into three groups. The high progesterone (high P) group received a subcutaneous implant of a silastic packet (50 x 70 mm) containing progesterone, and the low progesterone (low P) group received a similar implant of a small packet (25 x 40 mm) containing progesterone. The control (non-P) group received no treatment with exogenous progesterone. Blood samples were collected daily throughout the experiment for the analysis of gonadal steroid hormone levels and at 10-min intervals for 8 h on Days 0, 3, and 7 (Day 0: just before progesterone treatment) for analysis of the pulsatile frequency of LH secretion. Then estradiol was infused into the jugular vein of all animals at a rate of 3 microg/h for 16 h on Day 8 to determine whether an LH surge was induced. Blood samples were collected every 2 h from 4 h before the start of the estradiol infusion until 48 h after the start of the infusion. In each group, the mean +/- SEM concentration after progesterone implant treatment was 3.3 +/- 0.1 ng/ml for the high P group, 1.1 +/- 0.1 ng/ml for the low P group, and <0.1 ng/ml for the non-P group, concentrations similar to the luteal levels, subluteal levels, and follicular phase levels of the normal estrous cycle, respectively. The estradiol concentration ranged from 4 to 8 pg/ml after estradiol capsule implants in all groups. The LH pulse frequency was significantly (P < 0.05) suppressed on Day 3 (6.2 +/- 0.5 pulses/8 h) and on Day 7 (2.6 +/- 0.9 pulses/8 h) relative to Day 0 (9.0 +/- 0.5 pulses/8 h) in the high P group. In both the low P and non-P groups, however, the changes of pulsatile frequency of LH were not significantly different, and high pulses (7-9 pulses/8 h) were maintained on each of the 3 days they were tested. An LH surge (peak concentration, 100.3 +/- 11.0 ng/ml) occurred in all goats in the non-P group, whereas there was no surge mode secretion of LH in either the high P or the low P group. The results of this study support our hypothesis that the threshold levels of progesterone that regulate negative feedback action on the LH pulse and the LH surge are different. Low levels of progesterone, around 1 ng/ml, completely suppressed the LH surge but did not affect the pulsatile frequency of LH secretion.

Animals↗
PubMed1986

Plasma progesterone levels during pregnancy in the little brown bat Myotis lucifugus (Vespertilionidae).

Plasma progesterone was measured by radioimmunoassay in individual female Myotis lucifugus throughout pregnancy and lactation. Progesterone levels, which averaged 6.7 +/- 0.7 ng/ml in late hibernation, rose to a mean of 18.9 +/- 6.7 ng/ml in unimplanted bats collected in the first two weeks after arrival at a maternity roost. Analysis of progesterone levels in bats in which the developmental stage of the embryo was known revealed two sharp, transient increases in plasma progesterone during the preimplantation period. The first, with values of 30-45 ng/ml, occurred at ovulation. The second, with values of 20-30 ng/ml, coincided with blastocyst formation. Progesterone levels increased exponentially from a mean of 7.4 +/- 1.0 ng/ml during early implantation to peak values of 100-200 ng/ml (means = 136.2 +/- 15.6) in the last two weeks of pregnancy, and showed no evidence of either a midpregnancy or prepartum decline. Despite involution of the corpus luteum at the end of pregnancy, progesterone levels averaged 9.0 +/- 1.0 ng/ml during lactation and did not decline until the end of lactation. In bats undergoing abortion, mean levels of plasma progesterone were already less than 6 ng/ml, equivalent to levels in nonbreeding females. The results indicate that the progesterone profile of pregnant M. lucifugus, though generally resembling those of other bats, exhibits several distinctive features. The sharp rise in plasma progesterone coinciding with blastocyst formation has not been reported in other mammals and suggests a possible role of progesterone in the cavitation process. In addition, peak values of plasma progesterone in late pregnancy were conspicuously higher than levels reported in other verpertilionid bats. The levels did not appear to fall before parturition, although such falls have been reported in other bats.

Acclimatization↗
PubMed1989

The metabolic clearance of progesterone in the pregnant rat: absence of a physiological role for the lung.

The metabolic clearance rate (MCR) of progesterone is among the highest for all steroid hormones studied, yet it is difficult to apportion this high MCR to specific organ contributions. The isolated lung has been shown to metabolize progesterone, and since this tissue receives the entire cardiac output, potentially it could make a major contribution to the overall MCR. This possibility was examined in the present study by measuring lung extraction of [3H]progesterone under steady-state conditions in the intact pregnant rat. Anesthetized rats (n = 6) were infused with [3H]progesterone via a femoral vein for 100 min on Day 16 of pregnancy. After the onset of steady state (40 min), four blood samples were obtained at 20-min intervals from the right ventricle and from the aorta, and the concentrations of [3H]progesterone and its metabolites were determined. Throughout the sampling period, mean arterial pressure and heart rate remained stable (two-way analysis of variance), as did the production rate (3.76 +/- 0.35 mg/day; mean +/- SEM) and the MCR (34.8 +/- 3.5 ml/min) of progesterone. Despite this high rate of clearance, there was no difference between the concentration of [3H]progesterone in arterial and right ventricular blood, indicating no net extraction of progesterone during passage through the lung. Furthermore, there was no change in the concentration of either lipid-soluble or aqueous-soluble [3H]progesterone metabolites during trans-lung passage. These observations demonstrate that the lung does not contribute to the MCR of progesterone when measured under physiological and steady-state conditions. Therefore, the relationship, MCR (ml/min) = whole-body extraction (%) x cardiac output (ml/min), is upheld for progesterone in the rat.

Animals↗
PubMed1995

Relationship of circulating steroid hormones, luteal luteinizing hormone receptor and progesterone concentration, and embryonic mortality during early embryogenesis in the domestic cat.

Serum hormones, corpus luteum (CL) progesterone, and CL LH receptors were characterized and interrelated to ovarian follicle and CL number and preimplantation embryo quality/survival in the cat. Blood samples were collected from queens ovariohysterectomized at 64 (n = 7), 76 (n = 11), 100 (n = 8), 124 (n = 7), 148 (n = 6), or 480 (n = 8) h after first copulation (3-times-daily matings on Days 2 and 3 of estrus). Ovarian CL were enucleated, weighed, and bisected; one hemi-CL was assayed for progesterone and the other for LH receptors. Serum was assessed for estradiol-17 beta and progesterone. Serum estradiol-17 beta concentrations did not return (p > 0.05) to baseline approximately 20 pg/ml) until 124 h after first copulation, whereas serum progesterone began to increase (> 1 ng/ml) by 76 h, was elevated (p < 0.05) by 124 h, and continued to rise thereafter. Serum progesterone was highly correlated with CL mass and LH receptor and progesterone concentration (range, r = 0.69-0.82; p < 0.01). CL progesterone and LH receptor concentrations were similar (p > 0.05) at 64 and 76 h, and both increased (p < 0.05) at subsequent time intervals and were correlated closely (r = 0.65; p < 0.01). Although ovarian CL were distinct and well organized by 64 h, pronounced elevations in serum progesterone and CL LH receptors and progesterone did not occur until at least 36 h later. The rapid increase in serum progesterone concentrations between 100 and 148 h was related to accelerated LH receptor synthesis and CL progesterone production and not entirely to enhanced CL growth.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗