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PubMed1986

Lipoprotein-stimulated and estradiol-maintained progesterone secretion by dissociated rabbit luteal cells in vitro.

Elevated activity of 3-hydroxy-3-methyglutaryl coenzyme A reductase (HMG-CoA reductase) was observed in the rabbit ovary and corpus luteum during pregnancy. Based on this study, it was proposed that de novo cholesterol synthesis rather than the uptake of exogenous plasma cholesterol (lipoproteins) was of primary importance in providing steroid substrate for progesterone synthesis by the rabbit luteal cell. Using a perifusion system, the present study challenges this hypothesis by demonstrating that both low- and high-density lipoproteins (at protein concentrations of 100 micrograms/ml and 50 micrograms/ml, respectively) were able to acutely stimulate progesterone production by dissociated rabbit luteal cells. The increase in progesterone synthesis was due to increased cholesterol substrate and not to protein-enhanced progesterone release. The ability of luteal cells to respond to lipoproteins was dependent on both dose- and sequence of treatment, with high-density lipoprotein (HDL) being unable to stimulate progesterone production if preceded by perifusion with low-density lipoprotein (LDL) or HDL. In addition, 17 beta-estradiol appeared to regulate lipoprotein utilization by attenuating the LDL response after 1 h of perifusion. We conclude that lipoproteins may provide cholesterol substrate for progesterone biosynthesis in vitro and that 17 beta-estradiol, in addition to maintaining progesterone production by luteal cells, may also regulate lipoprotein utilization. Thus, maintenance of steady progesterone secretion in response to estradiol supercedes that of LDL-stimulated progesterone secretion by rabbit luteal cells in vitro. This study suggests an interaction between estrogen and lipoproteins that may prove physiologically important in regulating progesterone production by rabbit luteal cells in vivo.

Animals↗
PubMed1987

Evidence for the preferential utilization of esterified cholesterol in progesterone production by rabbit corpora lutea.

Our previous studies show that lipoproteins stimulate progesterone secretion by rabbit luteal cells in vitro and that estradiol modifies this effect. This study examines the relationship between estradiol and serum lipoproteins for progesterone production by rabbit corpora lutea in vivo. Using morphometric analysis, we determined that estrogen treatment of hysterectomized pseudopregnant (E-hyst) rabbits increased luteal lipid volume by mid-pseudopregnancy without altering serum progesterone levels. Treatment of E-hyst rabbits with 4-amino-3,4,pyrazolo pyrimidine (APP) during early to mid-pseudopregnancy reduced serum cholesterol levels without decreasing serum progesterone concentrations. However, 3-hydroxy-3 methyl glutaryl-CoA reductase activity was increased. Thus, in the presence of exogenous estrogen, serum cholesterol is esterified and stored rather than converted directly into progesterone. APP-treatment of E-hyst rabbits during late-pseudopregnancy, when estrogen receptor levels are low, increased serum progesterone levels and reduced intracellular lipid content. Thus, stored lipid is the primary source of cholesterol for progesterone synthesis. In addition, estrogen, via estrogen receptor, is important in maintaining steady progesterone output despite fluctuations in serum lipoprotein levels. A working model for cholesterol utilization by rabbit luteal cells is presented, which suggests that stored cholesterol esters, derived from both endogenous and exogenous sources, is the key source or cholesterol for progesterone production. Furthermore, we propose that estradiol regulates the uptake and storage of cholesterol and its rate of metabolism into progesterone.

Adenine↗
PubMed1987

The effects of progesterone on follicular growth in the rabbit ovary.

Studies were undertaken to measure the growth of follicles in the rabbit ovary during periods of elevated blood levels of progesterone. The progestin was increased in the blood by pregnancy or by implantation of progesterone pellets, which raised blood progesterone to near the levels measured during pregnancy. After 1, 2, 3, or 4 weeks of pregnancy or progesterone-pellet treatment, follicles of 1.0 mm external diameter or greater were dissected out of the ovaries and their external diameters were measured; then, each follicle was extracted for measurement of estradiol content. Blood levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were measured in these animals as well. Follicles up to 2.5 mm in diameter were found in the ovaries of nonpregnant and untreated animals while 1.8 mm was the maximal size found during pregnancy or progesterone-pellet treatment. Furthermore, both in pregnant and in progesterone-treated rabbits, the follicular estradiol content and concentration were significantly suppressed compared to follicles from untreated rabbits. The progesterone pellets had no major effect on the levels of LH and FSH in the blood; the concentration of these gonadotropins in the progesterone-treated rabbits was virtually identical to levels previously measured in the blood of pregnant animals. The results of these studies indicate that progesterone exerts an inhibitory action on follicular development and steroidogenic function in the rabbit ovary. The progesterone action appears to be exerted directly on the ovary and is not indirect, by way of an inhibition of gonadotropin secretion.

Animals↗
PubMed1988

Effects of progesterone and estradiol-17 beta on uterine secretion of prostaglandin F2 alpha in response to oxytocin in ovariectomized ewes.

Twenty ovariectomized ewes were used in an experiment designed to examine the interaction of progesterone, estradiol, and oxytocin in the regulation of uterine secretion of prostaglandin F2 alpha (PGF2 alpha). All ewes underwent a steroid pretreatment that mimicked the changes in progesterone and estradiol which occur during the six days immediately prior to estrus. After pretreatment, ewes were randomly assigned to 1 of 4 treatment groups: 1) control (n = 4); 2) estradiol-17 beta (n = 6); 3) progesterone (n = 4); and 4) progesterone and estradiol-17 beta (n = 6). Progesterone was injected twice daily for 15 days. The dose of progesterone varied with day postestrus in a manner designed to simulate endogenous luteal secretion of progesterone. Estradiol-17 beta was administered in s.c. Silastic implants. The implants maintained circulating concentrations of estradiol at 3 pg/ml. On Days 5, 10, and 15 of treatment, ewes were injected with oxytocin (10 IU in 1.0 ml saline, i.v.). Jugular venous blood samples were collected beginning one-half hour prior to and continuing for 2 hours post-oxytocin injection for quantification of 13,14-dihydro-15-keto-prostaglandin F2 alpha (PGFM). No changes in concentration of PGFM following injection of oxytocin were observed on Day 5 or 10 in any treatment group. Concentrations of PGFM increased following injection of oxytocin on Day 15 only in groups receiving progesterone. Both the area under the PGFM response curve (p = 0.08) and peak response (p = 0.06) were greater in ewes treated with progesterone and estradiol-17 beta than in those receiving progesterone alone.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Opioids modulate progesterone production in prepubertal Bunaji heifers.

The opioid antagonist naloxone was administered to prepubertal heifers, and its effects on progesterone, cortisol, and LH secretions were studied. Pooled pretreatment values in peripheral plasma for progesterone averaged 0.26 +/- 0.08 ng/ml (+/- SE), and those for cortisol averaged 13 +/- 1.2 ng/ml. Naloxone treatment at either 1.1 (Nal-1) or 2.0 (Nal-2) mg/kg BW significantly increased circulating progesterone within 15 min of i.v. injection, which was sustained for 45 and 75 min, respectively. Maximal progesterone concentrations were 1.8 +/- 0.16 ng/ml and 1.8 +/- 0.19 ng/ml at the low and high naloxone dosages; progesterone values were basal by 120 min. Naloxone caused a dose-dependent increase in plasma cortisol averaging 20 +/- 3.1, 28 +/- 4.2, and 49 +/- 5.7 ng/ml in the immediate 120 min posttreatment in control, Nal-1, and Nal-2 heifers, respectively; but naloxone injection, at either the low or the high dosage, had no effect on plasma LH concentration. The effect of naloxone on progesterone concentration was dependent on the age and body weight of the animal; it was first observed at 28 mo of age and between 130 and 160 kg BW. None of the heifers that showed transient elevations in progesterone exhibited estrous behavior or had a palpable CL throughout the study. These coincident transient increases in circulating progesterone and cortisol demonstrate that an endogenous inhibitory opioidergic system is involved in the control of steroid hormone secretion in prepubertal zebu heifers. Further, an adrenal source of this progesterone is indicated, but whether the progesterone participates in the induction of an LH increase in the prepubertal heifer is not clear.

Animals↗
PubMed1999

Human sperm chemotaxis: is progesterone a chemoattractant?

Follicular fluid (FF) induces sperm chemotaxis in human spermatozoa. Progesterone also causes sperm accumulation. However, sperm accumulation can be caused by chemotaxis, chemokinesis, and trapping of various kinds. It has been suggested that progesterone also induces chemotaxis in human spermatozoa. In view of the physiological significance of sperm chemotaxis in human fertilization and its potential clinical implications, it is important to determine unequivocally whether chemotaxis is induced by progesterone and, if so, whether progesterone in FF is the chemoattractant. To resolve these questions we looked for characteristic changes in the direction of sperm swimming toward pure progesterone as well as toward FF before and after progesterone removal. Progesterone caused sperm accumulation and hyperactivation-like motility, but it caused very few changes in the direction of sperm swimming that are characteristic of chemotaxis. Removal of progesterone (and other steroids) from FF by charcoal treatment abolished the sperm hyperactivation-like motility but not sperm chemotaxis. These results suggest that while progesterone might be a weak chemoattractant, it is not the major chemoattractant in FF. Progesterone probably causes human sperm accumulation mainly by inducing hyperactivation-like motility and, as a consequence, sperm trapping.

Chemotaxis↗
PubMed1999

Progesterone alters biliary flow dynamics.

OBJECTIVE: To test the hypothesis that progesterone alters sphincter of Oddi and gallbladder function and, therefore, bile flow dynamics. SUMMARY BACKGROUND DATA: Although the effects of progesterone on the biliary tract have been implicated in the increased incidence of gallstones among women, the specific effects of prolonged elevation of progesterone levels, such as occurs with contraceptive progesterone implants and during pregnancy, on the sphincter of Oddi and biliary flow dynamics are still incompletely understood. METHODS: Adult female prairie dogs were randomly assigned to receive subcutaneous implants containing either progesterone or inactive pellet matrix only. Hepatic bile partitioning and gallbladder emptying were determined 14 days later using 99mTc-Mebrofenin cholescintigraphy. RESULTS: Significantly less hepatic bile partitioned into the gallbladder in progesterone-treated than in control animals. The gallbladder ejection fraction was significantly reduced from 73+/-6% in controls to 59+/-3% in the progesterone-treated animals. The rate of gallbladder emptying was significantly reduced from 3.6+/-0.3%/minute to 2.9+/-0.1%/minute. CONCLUSIONS: Progesterone administered as subcutaneous implants alters partitioning of hepatic bile between gallbladder and small intestine and, therefore, gallbladder filling. Progesterone also significantly impairs gallbladder emptying in response to cholecystokinin. The effects of progesterone on the sphincter of Oddi and the gallbladder may contribute to the greater prevalence of gallstones and biliary motility disorders among women.

Animals↗
PubMed2003

Progesterone induces the proliferation of urothelial cells in an epidermal growth factor dependent manner.

PURPOSE: We have previously reported that estrogen induced proliferation of urothelial cells is modulated by nerve growth factor (NGF). In this study we investigated whether progesterone induces urothelial cell proliferation and whether this effect is modulated by NGF or by epidermal growth factor (EGF). MATERIALS AND METHODS: Experiments were performed using human urothelial cells immortalized by human papillomavirus E6. Cell proliferation was determined using the alamarBlue (Trek Diagnostic, Westlake, New York) assay. Human papillomavirus were seeded in 48-well plates. They were incubated with 5% alamarBlue and different concentrations of progesterone, EGF or NGF in the presence or absence of neutralizing EGF or NGF antibody, K252a (an inhibitor of trkA, the high affinity receptor for NGF), Ru-486 (an antagonist of progesterone and glucocorticoid receptor) or ZK 137 316 (a specific antagonist of progesterone receptor). Immunoblotting was performed using specific antibodies for progesterone receptor, glucocorticoid receptor or EGF receptor. EGF content in conditioned medium was determined by enzyme-linked immunosorbent assay. RESULTS: In the presence of 10 nM to 1 microM progesterone urothelial cell proliferation was significantly increased 8.6% to 51.1%. This effect was abolished by ZK137 316 or by Ru-486. Hydrocortisone also induced urothelial cell proliferation. This effect was blocked by Ru-486 but not by ZK137 316. In addition, progesterone stimulated urothelial cell proliferation was inhibited by neutralizing EGF antibody but not by NGF antiserum or K252a. We also found that EGF synthesis and release by urothelial cells was increased by exogenous progesterone. This effect of progesterone was inhibited by ZK 137 316. CONCLUSIONS: These findings indicate that progesterone has the capacity to induce urothelial cell proliferation through its cognate receptor and this effect is mediated by EGF but not by NGF.

Carbazoles↗
PubMed1995

In vitro fertilization and the effect of progesterone and 17 alpha-hydroxyprogesterone on acrosome reaction of mouse epididymal spermatozoa.

This study assessed the effect of progesterone and 17 alpha-hydroxyprogesterone (17 alpha-OH-progesterone) at concentrations of 0.01-10 micrograms/ml, on the acrosome reaction and in vitro fertilizing ability of mouse epididymal spermatozoa. Cumulus masses containing oocytes were cultured in Brinster's medium, to which were added capacitated epididymal spermatozoa which had been incubated in medium with various concentrations of progesterone or 17 alpha-OH-progesterone for 90 min. IVF success rate was assessed 20-24 h following insemination. Progesterone was found to increase the fertilization rate at the 1 microgram/ml and 10 microgram/ml concentrations while lower concentrations had no effect. However, 17 alpha-OH-progesterone failed to show any effect on fertilizing ability. Incubation of epididymal spermatozoa in medium containing 1 microgram/ml and 10 micrograms/ml progesterone significantly increased the acrosome reaction as monitored by a chlortetracycline fluorescence assay. 17 alpha-OH-progesterone, however, failed to show any effect on the acrosome reaction. The results suggest direct effects of progesterone, but not of 17 alpha-OH-progesterone, on fertilization and the acrosome reaction of mouse spermatozoa.

17-alpha-Hydroxyprogesterone↗
PubMed2005

Progesterone can block the preovulatory gonadotropin-releasing hormone/luteinising hormone surge in the ewe by a direct inhibitory action on oestradiol-responsive cells within the hypothalamus.

Elevated oestradiol concentrations during the follicular phase stimulate a surge in gonadotropin-releasing hormone (GnRH) and luteinising hormone (LH) concentrations, which leads to ovulation. Progesterone can block the oestradiol-induced GnRH/LH surge, but the mechanism that is involved is unclear. We examined the effect of progesterone on oestradiol-induced activation of cells within the ovine hypothalamus/preoptic area (POA) to determine: (i) in which regions progesterone acts to block the GnRH/LH surge and (ii) whether progesterone directly or indirectly prevents activation of oestradiol-responsive cells. Cellular activation was assessed by measuring the number of cells that expressed Fos (an immediate early gene). Exposure to increased oestradiol concentrations in the absence of progesterone (which normally stimulates a LH surge) did not cause any region-specific changes in hypothalamic Fos expression during the activation stage of the LH surge-induction process (Experiment 1). The same treatment significantly increased cellular activation within the POA, lateral septum (LS), and arcuate nucleus at the time of surge onset (Experiment 2). Concurrent exposure to increased oestradiol and progesterone concentrations during the activation stage of the surge-induction process (which normally blocks the LH surge) was associated with significantly reduced cellular activation within the ventromedial hypothalamus and anterior hypothalamic area, relative to the positive controls (oestradiol increment alone) and arcuate nucleus relative to the negative controls (no increment in oestradiol) during the activation stage (Experiment 1). At the time of surge onset (Experiment 2), exposure to progesterone during the activation period prevented the oestradiol-induced increase in cellular activation that occurred in the POA, LS and arcuate nucleus of the positive controls. These results demonstrated that oestradiol and progesterone induced differential region- and time-specific effects on cellular activation within the regions of the ovine brain that generate the preovulatory GnRH/LH surge. Moreover, the lack of cellular activation within the POA, LS and arcuate nucleus at the time of surge onset in animals exposed to progesterone during the activation stage is consistent with the hypothesis that progesterone can block the preovulatory surge by direct inhibition of oestradiol-induced cellular activation in these areas.

Animals↗
PubMed1998

Assessment of progesterone-induced acrosome reaction by biotinylated monoclonal antibody probes.

PROBLEM: To develop an immunohistochemical assay for determination of acrosome-reacted human sperm and to study the effects of progesterone and cholesterol treatment on human sperm acrosome reaction. METHOD OF STUDY: Three distinct anti-sperm monoclonal antibodies were biotinylated and used as probes for assessment of acrosome reaction in a 30-min immunohistochemical assay. Progesterone and/or cholesterol were added to sperm preparation to influence the acrosome reaction in different experimental conditions. RESULTS: Percentages of acrosome-intact sperm decreased significantly during the 18-hr incubation. Acrosome reaction could be induced by progesterone as early as 2 hr after sperm incubation in human tubal fluid. The degree of progesterone-induced acrosome reaction was time dependent and the optimal effect was reached by adding 10 micrograms/ml progesterone for 30 min incubation. Progesterone-induced acrosome reaction was shown to be hormone-concentration dependent with 50% stimulation at 1 microgram/ml. Cholesterol (1 microgram/ml) was found to inhibit progesterone-induced acrosome reaction either by co-incubation with human sperm during capacitation, or by simultaneous incubation with progesterone during acrosome reaction induction. CONCLUSIONS: Assessment of human sperm acrosomal status by avidin-biotin immunohistochemical assay can be a routine in clinical laboratories for male infertility services. Cholesterol can inhibit progesterone-induced acrosome reaction, possibly by its modifications of sperm plasma membrane and/or interference of progesterone binding to its surface receptors.

Acrosome↗
PubMedDate not supplied

Progesterone and cell-cell adhesion interact to regulate rat granulosa cell apoptosis.

Ovarian follicles are composed of both small and large granulosa cells, but only the large granulosa cells undergo apoptosis within 24 h of culture in serum-free medium. The present study was designed to assess the relationship between cell-cell contact, progesterone treatment, and granulosa cell apoptosis. For this study, individual large granulosa cells were isolated from immature rat ovaries after sequential incubation with EGTA and EGTA-sucrose solutions. Granulosa cells were then cultured for 24 h in RPMI-1640 (control) supplemented with progesterone and (or) the progesterone antagonist RU 486. The cells were then fixed and assessed for apoptosis by either electron microscopy or in situ end labeling of DNA fragments. After 24 h of culture, the proportion of apoptotic granulosa cells was twofold lower for aggregated cells compared with single granulosa cells (p < 0.05). Aggregated granulosa cells were observed to be connected by gap junctions. Compared with controls, progesterone reduced and RU 486 increased the percentage of single and aggregated apoptotic granulosa cells present after culture. In the presence of RU 486, progesterone reduced the percentage of apoptotic single granulosa cells from 84 +/- 4% (RU 486 alone) to 66 +/- 8%. In granulosa cell aggregates, progesterone reduced the incidence of apoptosis from 86 +/- 3% to 44 +/- 7% (p < 0.05). Progesterone in the presence of RU 486 was more effective in inhibiting apoptosis of aggregated granulosa cells than in single granulosa cells (p < 0.05). Taken together, these data indicate that (i) progesterone acts through the progesterone receptor to inhibit granulosa cell apoptosis and (ii) cell-cell adhesion enhances progesterone's anti-apoptotic actions.

Animals↗
PubMed1984

Androgen inhibition of FSH-stimulated progesterone production by granulosa cells of prepubertal pigs.

Androgens have been reported to stimulate progesterone production by granulosa cells of several species, and to act synergistically with FSH in stimulation of progesterone accumulation by rat granulosa cells. Studies were undertaken to examine the effect of androgens on FSH-stimulated progesterone production in culture by granulosa cells derived from prepubertal pig ovaries. When included in 24-h culture with FSH, both androstenedione and testosterone caused a reduction in progesterone accumulation, but dihydrotestosterone and androsterone did not. Granulosa cells were cultured for 24 h with FSH and [14C]progesterone with or without testosterone; testosterone did not affect the rate of overall metabolism of [14C]progesterone and it was therefore concluded that testosterone inhibited progesterone synthesis, rather than enhancing its catabolism. 17 beta-Estradiol also inhibited FSH-stimulated progesterone accumulation. To determine whether the action of testosterone was mediated by conversion to estradiol, granulosa cells were cultured with FSH and testosterone with or without an aromatase inhibitor (4-acetoxy-androstenedione). The aromatase inhibitor failed to prevent the testosterone-induced reduction in progesterone accumulation, although it markedly inhibited estradiol accumulation. These results indicate that theca-derived androgens can inhibit FSH-stimulated progesterone production by granulosa cells in the prepubertal pig, independently of estradiol.

Androgens↗
PubMed1985

Inhibition of progesterone secretion by a 3 beta-hydroxysteroid dehydrogenase inhibitor in late pregnant sheep.

The role of progesterone in the initiation of parturition in the sheep is unclear. Whether a decrease in plasma progesterone is the essential prerequisite for the initiation of parturition or whether other factors also maintain uterine quiescence until delivery is not known. The effect of withdrawal of progesterone on the initiation of parturition has been investigated by intravenous administration of trilostane, a 3 beta-hydroxysteroid dehydrogenase delta 5-4 isomerase inhibitor, to late pregnant sheep. Twenty-five or 100 mg trilostane caused a precipitous decrease in plasma progesterone to about 30% of preinjection levels. Progesterone remained depressed for up to 7 days after treatment. 13,14-Dihydro-15-keto-prostaglandin F2 alpha (PGFM) became elevated between 7 and 36 h after trilostane injection but gradually returned to preinjection levels during the subsequent 36 h, at a time when plasma progesterone was still depressed. Four of 11 animals treated with 100 or 200 mg trilostane aborted prematurely at a time when plasma PGFM was maximal and plasma progesterone minimal. There were no consistent changes in plasma estradiol-17 beta or ovine placental lactogen concentrations after treatment with trilostane. It is suggested that a decrease in plasma progesterone will cause a transient increase in plasma PGFM concentrations which can lead to the premature initiation of parturition. In some instances the myometrium does not appear to respond to the elevated PGFM concentrations even when the estrogen:progesterone ratio is elevated by a decrease in plasma progesterone.

3-Hydroxysteroid Dehydrogenases↗
PubMed1990

Effect of estrogen and progesterone on metabolism of apoprotein B in baboons.

To determine the metabolic mechanisms by which estrogen and progesterone alter levels of apoprotein B (apo B)-containing lipoproteins, 12 ovariectomized and hysterectomized baboons, maintained on a high-cholesterol (1.7 mg/kcal) and a high-fat (40% from lard) diet and divided into four groups, were treated with estrogen, progesterone, estrogen plus progesterone, and a placebo. After 12 wk, plasma cholesterol was unchanged in the control and progesterone groups but was reduced in the estrogen- and estrogen plus progesterone-treated groups. The reduction was primarily because of decreased low-density lipoprotein (LDL) cholesterol. LDL apo B levels decreased parallel to the LDL cholesterol. Very low-density lipoprotein (VLDL) and LDL apo B metabolism were studied using a double-label turnover study. Multicompartmental modeling suggested that LDL apo B was kinetically heterogeneous and that there exists an extravascular pool, perhaps consisting of hepatic remnants, that contributes significantly to LDL apo B transport. The model was used to estimate apo B production rates and residence times. VLDL apo B production was not affected by estrogen but was increased by progesterone. LDL apo B production was increased by both estrogen and progesterone. The residence time of LDL apo B was decreased by estrogen and estrogen plus progesterone but not by progesterone. Thus estrogen and progesterone have independent effects on apo B metabolism in baboons.

Animals↗
PubMedDate not supplied

Interaction of prostaglandin F(2alpha) and prostaglandin E(2) on progesterone production in human granulosa-luteal cells.

This study examined the effects of prostaglandin-F(2alpha) (PGF(2alpha)), prostaglandin-E(2) (PGE(2)) and their interactions on progesterone production in human granulosa-luteal cells (GLCs). Human GLCs collected from in vitro fertilization patients were cultured for 1 (D(1)) or 8 days (D(8)), followed by a 24-hour treatment period, after which media were collected and radioimmunoassayed for progesterone. Seven-point PGF(2alpha) and PGE(2) concentration-response curves were crossed into a matrix of 49 separate treatments. Responses were plotted in three dimensions and as two-dimensional "slices". In D(1) cultured human GLCs neither PGF(2alpha) nor PGE(2) alone had any effect on progesterone production, however two different combinations of these hormones led to at least a 3-fold increase in progesterone production. This stimulation was seen when cells were treated with 10(-6) M PGF(2alpha) plus 10(-9) M PGE(2), and when they were treated with 10(-10) M PGF(2alpha) plus 10(-9) M PGE(2). In D(8) GLCs, PGF(2alpha) stimulated progesterone production maximally at 10(-9) M, while the lowest (10(-11) M) and highest concentrations (10(-6) M) tested were ineffectual. On the contrary, in the presence of high concentrations of PGE(2) (10(-6) to 10(-7) M), PGF(2alpha)-mediated stimulation of progesterone production was attenuated. In a similar fashion to PGF(2alpha), PGE(2) also acted in a luteotrophic manner, although the maximal stimulation of progesterone production was seen at a higher concentration (10(-8) to 10(-7) M). Likewise, PGE(2)-mediated progesterone production was attenuated by the presence of high concentrations of PGF(2alpha) (10(-6) to 10(-7) M). In conclusion, in D(1) human GLCs neither PGF(2alpha) nor PGE(2) alone were luteotrophic, although specific combinations of these hormones were. Conversely, in D(8) GLCs both PGF(2alpha) and PGE(2) stimulated progesterone production in a biphasic manner, while the presence of a high concentration of either of these prostaglandins attenuated the luteotrophic effects of the other. Therefore, PGF(2alpha) and PGE(2) interacted in a concentration-dependent manner, resulting in a multimodal progesterone response, which was easily visualized using three-dimensional plots.

Cells, Cultured↗
PubMed1976

Suckling and LH-induced progesterone secretion in lactating hamsters (Mesocricetus auratus).

The effects of suckling and LH upon serum progesterone levels in lactating hamsters were investigated. Diurnal rhythms in serum levels of progesterone and LH occur throughout lactation in the hamster and these levels are normally higher between 15.00 and 17.00 than between 8.00 and 12.00 (lights on 6.00-20.00). Hamsters injected with 10 mug of LH at 8.00 on day 9 of lactation had higher levels of serum progesterone 2 h after injections than did vehicle-injected controls. Suckling was also found to induce an increase in serum progesterone concentrations. 30 min of suckling from 10.30 to 11.00 on days 10 or 11 of lactation resulted in increased serum levels of progesterone and prolactin, but had no measurable effect upon serum LH levels in animals bled at 11.00. However, suckling for 30 min from 15.00 to 15.30 had no effect upon serum progesterone levels, although it did result in increased titers of both serum LH and prolactin at 15.30. Ovariectomy on day 7 of lactation resulted in lowered levels of serum progesterone at 11.00 on day 11 of lactation and abolished the suckling-induced increase in serum progesterone concentrations. These findings suggest that in the lactating hamster (1) suckling bouts stimulate progesterone secretion from the ovaries, and (2) the diurnal rise in serum progesterone levels is stimulated in part by the increase in serum levels of LH.

Animals↗
PubMed1992

Progesterone promotes rapid desensitization of alpha 1-adrenergic receptor augmentation of cAMP formation in rat hypothalamic slices.

We previously demonstrated that norepinephrine (NE) induction of cAMP accumulation in slices of the preoptic area (POA) and middle hypothalamus (MH) is reduced by in vivo administration of progesterone to estradiol-primed rats, apparently by eliminating alpha 1-receptor augmentation of beta-receptor-stimulated cAMP formation. The present studies examined whether in vitro exposure to progesterone would also depress NE-stimulated cAMP synthesis. POA and MH slices from estradiol-primed females were incubated with 20 nM progesterone for 5-30 min prior to addition of 100 microM NE. Pre-incubation of slices with progesterone for as little as 5 min significantly suppressed NE-stimulated cAMP formation by greater than 60%. This effect was estrogen-dependent in that progesterone in vitro did not inhibit NE-stimulated cAMP accumulation in slices from ovariectomized rats not pretreated with estradiol. Isoproterenol, a beta-adrenergic agonist, elevated cAMP to the same extent in slices from estradiol-primed females incubated with and without progesterone in vitro; however, the alpha 1-agonist, phenylephrine, was unable to augment cAMP formation in slices incubated in vitro with progesterone for 5 min prior to drug challenge. To determine whether the rapid effects of progesterone may be exerted at the level of the plasma membrane, we employed progesterone conjugated to bovine serum albumin at carbon 3 (P-3-BSA). Slices from estradiol-primed rats incubated with P-3-BSA for 5 min did not exhibit an alpha 1-receptor augmentation of beta-receptor-stimulated cAMP accumulation. These data indicate that progesterone may have rapid, non-genomic effects on alpha 1-adrenergic receptor coupling to second-messenger systems in the hypothalamus of female rats.

Animals↗