Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PROGESTERONE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,135 records · Page 63Linked to original sources
PubMed2006

Mechanism of progesterone neuroprotection of rat cerebellar Purkinje cells following oxygen-glucose deprivation.

The survival of rat Purkinje cell (PCs) cerebellar cultures was used to test the hypothesis that progesterone is protective against oxygen-glucose deprivation through potentiation of GABA(A) receptor activity. Electrophysiological recordings confirm that PCs develop robust excitatory and inhibitory synapses in culture. Exposure of cultured PCs to increasing concentrations of progesterone during oxygen-glucose deprivation revealed a concentration-dependent protection by progesterone, with significant protection observed at physiological concentrations, as low as 10 nm. The concurrent application of the GABA(A) receptor antagonist picrotoxin (100 microm) completely abolished the neuroprotection afforded by progesterone, indicating that progesterone is neuroprotective through activation of GABA(A) receptors. Progesterone potentiates GABA(A) receptor activity indirectly through its metabolites, such as allopregnanolone (ALLO). Therefore, ALLO was applied to PC cultures and was observed to produce significant protection at all concentrations tested, from 10 to 1000 nm. Finally, the inhibition of progesterone metabolism with finasteride abolished the protection afforded by progesterone without having any effect on the neuroprotection caused by ALLO. These data indicate that progesterone protects cerebellar PCs at physiological concentrations through a GABA-active metabolite.

Animals↗
PubMed1982

Plasma progesterone in the umbilical vessels at vaginal delivery of term infants.

The influence of stress and related factors on umbilical-cord vessel progesterone concentrations have been investigated in 150 vaginal deliveries. Cord vein progesterone levels were greater in breech deliveries than in forceps deliveries and in vaginal deliveries by maternal effort alone. Within the forceps group there was no difference in cord vessel progesterone concentrations between lift-out, mid-cavity or rotational forceps deliveries. Levels of progesterone were significantly greater in forceps deliveries where the infant was clinically distressed (P less than 0.01). Similarly, within the normal group progesterone levels were greater in a stressed group of infants, where cord vein pH, artery pH, Apgar score at 1 min or birthweight fell below the 10th centile for the study group. No differences in plasma progesterone concentration were found with labour commencing spontaneously or by induction, nor did the sex of the infant appear to influence this hormone. Progesterone levels were higher in samples from primiparae than in those from multiparae due to a small number of primiparae who had excessively long labours and high progesterone concentrations. There was, however, no strong statistical correlation between length of labour and progesterone concentrations.

Breech Presentation↗
PubMed1986

Skin graft survival in the uterine lumen of ewes treated with progesterone.

An experiment was conducted to determine the effect of progesterone on survival of skin transplants placed in the uterine lumen of ovariectomized ewes. Animals were treated for 30 days with either a corn oil vehicle (n = 4) or progesterone at 50 (n = 3) or 200 mg/day (n = 3). An autograft and allograft were then placed in each uterus, and treatments were continued for an additional 30 days before grafts were examined for survival. All autografts were present 30 days after grafting and most appeared healthy upon histological examination. Allografts placed into the uterine lumen of progesterone-treated ewes were present 30 days after grafting but were necrotic in histological appearance. Allografts placed within the uterus of corn oil-treated ewes were completely resorbed. Uterine secretions that accumulated in the uterine lumen were examined for inhibitory effects on [3H-methyl]thymidine incorporation by lymphocytes stimulated with phytohemagglutinin (PHA). The total amount of immunosuppressive activity in the uterine lumen was greater (P less than 0.05) for progesterone-treated ewes than for corn oil-treated ewes. Concentrations of progesterone in uterine secretions of progesterone-treated ewes ranged from 0.3 to 3.4 ng/ml. Thymidine incorporation into PHA-stimulated lymphocytes was not affected by in vitro treatment with up to 500 ng/ml of progesterone. In conclusion, progesterone delayed resorption of skin allografts placed in the uterine lumen. Results are consistent with the hypothesis that progesterone mediated this effect by stimulating the secretion of immunosuppressive substances into the uterine lumen.

Animals↗
PubMed1971

The contribution of the adrenal gland to the total amount of progesterone produced in the female rat.

1. The amount of progesterone contained in both adrenal glands of a rat was similar to or larger than the amount of progesterone in the ovaries of the same rat. This was found in unstressed rats, in stressed rats and also in pregnant rats.2. After ether anaesthesia and exsanguination the adrenal progesterone content was increased by 75%; the ovarian progesterone content remained unchanged.3. In contrast, prolonged operative stress resulted in a rise in the ovarian content of progesterone and 20-dihydroprogesterone whereas the adrenal progesterone content of these rats was lower than that of unstressed rats.4. The rate at which progesterone was secreted by the adrenal glands of stressed rats was similar to the ovarian progesterone secretion rate. Rats which were kept under mild stress conditions before the experiment showed higher adrenal progesterone secretion rates.

Adrenal Glands↗
PubMed1991

Inhibition of glucose metabolism by progesterone in adipocytes: role of protein synthesis.

Progesterone decreases [I-14C]glucose oxidation in isolated female rat adipocytes within 20 min of incubation. Because steroids regulate transcription mechanisms, the relationship between protein synthesis and glucose metabolism was studied in the presence of progesterone. Actinomycin D does not affect basal glucose oxidation or the progesterone effects on it; cycloheximide and puromycin decrease basal glucose oxidation, but only puromycin decreases the inhibitory progesterone effect. Although puromycin inhibits glucose transport, the common site of action of puromycin and progesterone does not seem to be glucose transport, which, as we showed previously, is not modified by the steroid. Incorporation of [3H]leucine into acid-precipitable proteins is decreased by puromycin and cycloheximide but not by actinomycin D or progesterone; moreover, the action of these inhibitors does not change in the presence of the steroid. As shown by electrophoresis (SDS-PAGE) and autoradiography, L-leucine is incorporated into adipocyte proteins as early as 20 min and progesterone increases this incorporation into five proteins. Leucine is a ketogenic amino acid that is also incorporated into lipids; progesterone depresses L-leucine incorporation into fatty acids by a glucose-dependent mechanism. These results suggest that the inhibitory effect of progesterone on glucose metabolism is related to an enhanced protein synthesis counterbalanced by decreased fatty acid synthesis.

Adipose Tissue↗
PubMed1991

Progesterone and modulation of endothelium-dependent responses in canine coronary arteries.

Chronic treatment with estrogens enhances some endothelium-dependent relaxations. Whether or not progesterone would exert a similar effect is unknown. Experiments were designed to determine the effect of chronic treatment with progesterone on endothelium-dependent responses. Adult female dogs were ovariectomized and pellets containing carrier substance, estrogen, progesterone, or estrogen plus progesterone were implanted subcutaneously. After 14-21 days coronary arteries were removed, cut into rings, and suspended for the measurement of isometric force in organ chambers in the presence of indomethacin. Endothelium-dependent relaxations to ADP, bradykinin, or the calcium ionophore did not differ among groups. However, relaxations to acetylcholine and to the alpha 2-adrenergic agonist BHT-920 were greater in the estrogen-treated group than in the estrogen plus progesterone-treated group. In rings without endothelium, relaxations to nitric oxide and isoproterenol did not differ among groups. However, relaxations of the smooth muscle to ADP were greater in the progesterone-treated group than in the progesterone plus estrogen group. These results suggest that progesterone alone minimally affects endothelium-dependent responses. However, progesterone seems to antagonize the stimulatory effects of estrogen on two endothelium-dependent responses that are associated with pertussis toxin-sensitive guanine nucleotide regulatory proteins and the production of nitric oxide. These studies suggest that a specific receptor/second messenger system can be modulated by female reproductive steroid hormones.

Acetylcholine↗
PubMed1990

Effects of estrogen and progesterone on carotid body neural output responsiveness to hypoxia.

Pregnancy increases ventilatory and carotid body neural output (CBNO) responsiveness to hypoxia in cats (J. Appl. Physiol. 67: 797-803, 1989). To determine whether progesterone and estrogen stimulated hypoxic ventilatory and CBNO responsiveness, we studied 24 castrated male cats before and after 1 wk of placebo, estrogen, progesterone, or estrogen plus progesterone treatment. Estrogen plus progesterone treatment decreased end-tidal PCO2 (-3.8 +/- 0.8 Torr) and increased hypoxic ventilatory responsiveness, whereas estrogen or progesterone alone had no effect. Animals receiving progesterone alone or in combination with estrogen had higher CBNO responsiveness than placebo or estrogen-treated animals (shape parameter A = 45 +/- 7 vs. 27 +/- 4, P less than 0.05). However, the group treated with estrogen plus progesterone did not have greater CBNO responsiveness to hypoxia than the group receiving progesterone alone. The cross plot of the simultaneously measured CBNO and ventilation during progressive hypoxia revealed a greater slope in the estrogen-treated than in the placebo animals, suggesting that estrogen treatment increased central nervous system transduction of CBNO into ventilation. Thus the data taken together suggested that progesterone and estrogen had a combination of peripheral (carotid body) and central sites of action such that the administration of both hormones together had a more consistent stimulatory effect on hypoxic ventilatory responsiveness than either hormone alone.

Animals↗
PubMed1992

Central neural mechanisms of progesterone action: application to the respiratory system.

Around the turn of the century, it was recognized that women hyperventilate during the luteal phase of the menstrual cycle and during pregnancy. Although a causative role for the steroid hormone progesterone in this hyperventilation was suggested as early as the 1940s, there has been no clear indication as to the mechanism by which it produces its respiratory effects. In contrast, much mechanistic information has been obtained over the same period about a different effect of progesterone, i.e., the facilitation of reproductive behaviors. In this case, the bulk of the evidence supports the hypothesis that progesterone acts via a genomic mechanism with characteristics not unlike those predicted by classic models for steroid hormone action. We recently, therefore, undertook a series of experiments to test predictions of those same models with reference to the respiratory effects of progesterone. Here we highlight the results of those studies; as background to and precedent for our experiments, we briefly review previous work in which effects of progesterone on respiration and reproductive behaviors have been studied. Our results indicate that the respiratory response to progesterone is mediated at hypothalamic sites through an estrogen- (E2) dependent progesterone receptor- (PR) mediated mechanism requiring RNA and protein synthesis, i.e., gene expression. The E2 dependence of the respiratory response to progesterone is likely a consequence of the demonstrated induction of PR mRNA and PR in hypothalamic neurons by E2. In short, we found that neural mechanisms underlying the stimulation of respiration by progesterone were similar to those mediating its reproductive effects.

Animals↗
PubMedDate not supplied

Estrogen induces de novo progesterone synthesis in astrocytes.

The brain is an established target for peripheral steroids, but also expresses steroidogenic enzymes and is capable of de novo 'sex' steroid synthesis (neurosteroidogenesis) independent of peripheral steroidogenic organs. In adrenalectomized and ovariectomized rats that do not have peripheral sources of steroids, estrogen treatment increased progesterone levels specifically in the hypothalamus, indicating that estrogen stimulates progesterone neurosteroidogenesis. Recent studies have demonstrated that specific cell types preferentially secrete specific steroids, and that astrocytes are the primary progesterone synthesizing cells in the nervous system. We hypothesized that estrogen could directly induce de novo synthesis of progesterone in astrocytes. To determine whether estrogen stimulates progesterone synthesis in astrocytes, astrocyte-enriched cultures were grown to confluence, then grown for an additional 48 h in an estrogen- and phenol-free Dulbecco's Modified Eagle Medium (DMEM) and then treated with either 17beta-estradiol or steroid-free media. After culturing for 48 h in steroid-free, phenol red-free DMEM, low levels of progesterone were detected in the media, whereas progesterone levels were significantly increased in the media of astrocytes cultured in DMEM with 17beta-estradiol (10(-7)-10(-4)M). To determine whether estrogen regulated the mRNA expression of progesterone synthetic enzymes, P-450 side-chain cleavage and 3beta-hydroxysteroid dehydrogenase, control and 17beta-estradiol-treated astrocytes were harvested and prepared for Northern and slot blot analysis. Expression levels of enzyme mRNAs were very low and 17beta-estradiol did not significantly increase mRNA levels of either steroidogenic enzyme. These results suggest that estrogen directly stimulated the de novo synthesis of neuroprogesterone in astrocytes, and demonstrate the potential for estrogen to regulate reproductive physiology and behavior through the paracrine actions of astrocyte-derived progesterone.

3-Hydroxysteroid Dehydrogenases↗
PubMed1985

Effects of progesterone on the pituitary responsiveness to, and priming effect of luteinizing hormone releasing hormone in female rats exposed to constant light.

We have investigated the role of progesterone in the mating-induced release of luteinizing hormone (LH) and ovulation in female rats exposed to a 60-day period of constant light (LL). Plasma LH and progesterone concentrations were increased after mating; plasma estradiol concentrations, although not increased after mating, were increased compared with the concentrations in female rats on light-dark (LD) exposure during diestrus, proestrus evening and estrus. Progesterone induced ovulation in about half the number of female rats exposed to long-term LL, and in these animals, there was a significant increase in pituitary responsiveness to luteinizing hormone releasing hormone (LHRH) 5 h after progesterone injection. The magnitude of the priming effect of LHRH was markedly increased 2 h after progesterone treatment. Treatment with sodium pentobarbitone (SP) 15 min before an injection of progesterone, blocked the increase in pituitary responsiveness to LHRH 5 h later, but treatment with SP 4 h before progesterone injection did not block the increase in the magnitude of the priming effect of LHRH. These results suggest that progesterone acts both at the brain and pituitary to facilitate LH release, and that the increase in plasma progesterone produced by mating is at least partly responsible for the LH surge induced by mating in LL rats.

Animals↗
PubMed1985

Effects of progesterone on hypothalamic and plasma LHRH.

The hypothalamic action of progesterone on the regulation of LH secretion was investigated in a rat model ideally suited for the study of progesterone effects under conditions in which the animal is sensitive to progesterone but does not have an estrogen-induced gonadotropin surge. Immature female rats were ovariectomized at 26 days of age and treated for 4 days with a subphysiological dose of 0.1 microgram/kg/day estradiol followed by the injection of either 0.8 or 3.2 mg/kg progesterone at 9.30 a.m. on day 5. Serum LH levels were significantly depressed below control and pretreatment values 30 min after either dose of progesterone. At this time, 0.8 mg/kg progesterone administration resulted in a significant increase in MBH-LHRH and plasma LHRH levels. In contrast, the administration of the 3.2 mg/kg dose of progesterone did not result in an increase in MBH-LHRH levels. By 2 p.m., rats receiving 0.8 mg/kg progesterone, but not those receiving 3.2 mg/kg progesterone, showed a significant increase in serum LH concentration and this elevation was maintained at 4 p.m. The increase in serum LH levels was preceded by a rise in MBH-LHRH levels by 1 p.m., followed by a fall at 2 p.m. The LH rise was maintained during the rise and replenishment of the MBH-LHRH by 3 p.m. Between 2 and 3 p.m. the replenishment of MBH-LHRH levels was accompanied by a fall in POA-LHRH levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Positive and negative modification of dexamethasone-mediated MMTV gp52 release by progesterone pretreatment of tumor cells.

Murine mammary tumor cells (C3H Mm5mt/cl) were grown in charcoal-stripped serum to examine the effects of hormonal treatments on the expression and release of the mouse mammary tumor virus (MMTV) envelope glycoprotein (gp52). The ability of progesterone to modify extracellular levels of soluble and virion-associated MMTV gp52 was tested singly and as a pretreatment prior to dexamethasone (DXS) stimulation. Single treatments with DXS or progesterone demonstrated that DXS was substantially more effective at elevating gp52 than progesterone; however, a small but significant increase in gp52 levels was noted after 72 h of progesterone treatment. Progesterone pretreatments at 10- to 100-fold excess of DXS altered subsequent DXS-stimulated gp52 levels. Progesterone effectively antagonized DXS and reduced gp52 levels to those of controls but this reduction was accomplished only at the lowest concentrations of DXS (10(-8) M) and shortest treatment interval (24h). While some pretreatment protocols of varied dose slightly reduced gp52 levels at a point in time after treatment, the majority of progesterone pretreatments at 10(-7), 10(-6), and 10(-5) M resulted in MMTV gp52 levels which were equal to and in many cases significantly greater than those obtained with DXS alone. The ability to augment DXS-stimulated gp52 levels with progesterone pretreatment suggests that, under certain hormonal conditions, gp52 expression and release from mouse cells may be progesterone-dependent as well as glucocorticoid-dependent.

Animals↗
PubMed1986

Influence of 20 alpha-dihydroprogesterone on progesterone output by human chorion explants.

The output of progesterone by explants of chorion incubated without exogenous precursor was increased in the presence of 20 alpha-dihydroprogesterone (20 alpha-diHP). We have now examined the nature of the 20 alpha-diHP effect. Explants of chorion were incubated with [3H]progesterone and 3 microM non-radiolabelled 20 alpha-diHP to examine the effect of 20 alpha-diHP on progesterone metabolism. Significantly more radioactivity remained as unmetabolized [3H]progesterone compared to chorion incubated in the absence of non-radiolabelled 20 alpha-diHP. There was also a decrease in the output of [3H]-20 alpha-diHP by the explants but no change in the output of a second metabolite of progesterone [3H]-5 alpha-pregnanedione. When explants were incubated with 20 alpha-diHP in the presence of the 3 beta-hydroxysteroid dehydrogenase inhibitor, trilostane, the output of progesterone was significantly greater than with explants incubated with trilostane but without addition of 20 alpha-diHP. Radiochemically pure [3H]progesterone was produced by explants of chorion incubated with [3H]-20 alpha-diHP. We conclude that 20 alpha-diHP may serve as substrate for chorionic progesterone production through 20 alpha-hydroxysteroid dehydrogenase. 20 alpha-diHP, formed from progesterone, may also exert product feedback inhibition on this enzyme.

20-alpha-Dihydroprogesterone↗
PubMed1996

Effect of estrogen and progesterone on the expression of hepatic and extrahepatic sterol 27-hydroxylase in baboons (Papio sp).

Sterol 27-hydroxylase plays an important role in cholesterol metabolism in hepatic and extrahepatic tissues. To determine whether female sex steroid hormones influence its expression, we measured plasma and hepatic 27-hydroxycholesterol, hepatic mRNA levels, activity of sterol 27-hydroxylase, and adrenal mRNA levels of this enzyme in baboons (n = 6 per group) treated with placebo, estrogen, estrogen + progesterone, and progesterone. We also measured hepatic cholesterol concentration and hepatic acyl coenzyme A:cholesterol acyltransferase (ACAT) activity to determine their relationship with hepatic sterol 27-hydroxylase activity. Plasma 27-hydroxycholesterol concentration was increased by estrogen and estrogen + progesterone and was negatively correlated with plasma (P = .090) and LDL (P = .026) cholesterol concentrations. Similarly, hepatic sterol 27-hydroxylase activity was increased by estrogen and estrogen + progesterone and was negatively correlated with plasma (P = .056) and LDL (P = .052) cholesterol concentrations but was positively correlated with hepatic and plasma 27-hydroxycholesterol concentrations (P < .001). Hepatic ACAT activity was increased by progesterone (P < .004) and was positively correlated with plasma (P = .002) and LDL (P = .009) cholesterol concentrations but was negatively correlated with hepatic sterol 27-hydroxylase activity (P = .035). Hepatic and adrenal gland mRNA levels for sterol 27-hydroxylase were increased by estrogen alone or in combination with progesterone (P < .05). Hepatic sterol 27-hydroxylase activity was positively correlated with hepatic mRNA levels (P < .001), an observation suggesting that estrogen increases the activity of sterol 27-hydroxylase by increasing its synthesis. Hepatic cholesterol concentration was not influenced by the hormone treatment. These observations suggest that estrogen alone or in combination with progesterone increases the synthesis of sterol 27-hydroxylase in hepatic and extrahepatic tissues, and the increased activity of hepatic sterol 27-hydroxylase resulting from the increased synthesis is associated with a hypolipidemic effect on plasma LDL levels. Furthermore, progesterone alone increases the hepatic ACAT activity, but given in combination with estrogen progesterone does not have the same effect on hepatic ACAT activity. The effect of estrogen on hepatic ACAT activity may be mediated by sterol 27-hydroxylase and its effect on cholesterol metabolism (decreased cholesterol synthesis and increased output of cholesterol in the bile) in liver.

Adrenal Glands↗
PubMed1977

Regulation of rabbit myometrial alpha adrenergic receptors by estrogen and progesterone.

The effects of estrogen and progesterone on uterine alpha-adrenergic receptors were investigated by direct receptor-binding studies. Immature female rabbits were primed with estrogen by intramuscular injections for 4 days. Other rabbits were primed with progesterone by injections of estrogen for 4 days followed by injections of progesterone for 4 days. The alpha adrenergic antagonist, [3H]dihydroergocryptine, was used to directly assess the number and affinity of alpha adrenergic receptors in membranes derived from estrogen-and progesterone-primed uteri. Membranes from estrogen-primed uteri contained 257 +/- 52 fmol of [3H]dihydroergocryptine-binding sites per mg protein whereas membranes from progesterone-primed uteri contained 83 +/- 11 fmol of of binding sites per mg protein. This reduction of alpha adrenergic receptor-binding sites by progesterone was statistically significant (P less than 0.02). In contrast, no significant difference in the binding site affinity was observed between the estrogen- and progesterone-primed groups. The progesterone-induced decrease in the number of uterine alpha adrenergic receptors provides a potential explanation for the reduced alpha adrenergic contractile response to epinephrine in the progesterone-primed myometrium.

Animals↗
PubMed2006

Estradiol stimulates progesterone synthesis in hypothalamic astrocyte cultures.

The brain synthesizes steroids de novo, especially progesterone. Recently estradiol has been shown to stimulate progesterone synthesis in the hypothalamus and enriched astrocyte cultures derived from neonatal cortex. Estradiol-induced hypothalamic progesterone has been implicated in the control of the LH surge. The present studies were undertaken to determine whether hypothalamic astrocytes derived from female neonatal or female postpubertal rats increased production of progesterone in response to an estradiol challenge. Estradiol induced progesterone synthesis in postpubertal astrocytes but not neonatal astrocytes. This estradiol action was blocked by the estrogen receptor antagonist ICI 182,780. Previously we had demonstrated that estradiol stimulates a rapid increase in free cytosolic Ca(2+) ([Ca(2+)](i)) spikes in neonatal cortical astrocytes acting through a membrane estrogen receptor. We now report that estradiol also rapidly increased [Ca(2+)](i) spikes in hypothalamic astrocytes. The membrane-impermeable estradiol-BSA construct also induced [Ca(2+)](i) spikes. Both estradiol-BSA and estradiol were blocked by ICI 182,780. Depleting intracellular Ca(2+) stores prevented the estradiol-induced increased [Ca(2+)](i) spikes, whereas removing extracellular Ca(2+) did not prevent estradiol-induced [Ca(2+)](i) spikes. Together these results indicate that estradiol acts through a membrane-associated receptor to release intracellular stores of Ca(2+). Thapsigargin, used to mimicked the intracellular release of Ca(2+) by estradiol, increased progesterone synthesis, suggesting that estradiol-induced progesterone synthesis involves increases in [Ca(2+)](i). Estradiol treatment did not change levels of steroid acute regulatory protein, P450 side chain cleavage, 3beta-hydroxysteroid dehydrogenase, and sterol carrier protein-2 mRNAs as measured by quantitative RT-PCR, suggesting that in vitro, estradiol regulation of progesterone synthesis in astrocytes does not depend on transcription of new steroidogenic proteins. The present results are consistent with our hypothesis that estrogen-positive feedback regulating the LH surge involves stimulating local progesterone synthesis by hypothalamic astrocytes.

Aging↗
PubMed1977

Gonadotropin-sensitive progesterone production by rhesus monkey luteal cells in vitro: a function of age of the corpus luteum during the menstrual cycle.

Progesterone production in vitro, in the presence and absence of exogenous gonadotropin, was examined in suspensions of luteal cells, isolated by collagenase digestion of rhesus monkeys corpus luteum at various stages of the menstrual cycle. Cells isolated during mid-luteal phase (days 15-19) of the cycle secreted progesterone for up to 6 h in vitro. Mid-luteal phase cells were responsive to physiologic concentrations of human chorionic gonadotropin (hCG), with progesterone production significantly (P less than 0.05) enhanced by as little as 0.1 ng hCG/ml. Maximal stimulation was obtained with 100 ng hCG/ml. Both macaque chorionic gonadotropin (mCG) and human luteinizing hormone (hLH) significantly (P less than 0.01) increased progesterone production, while human follicle stimulating hormone (hFSH) did not. Under control conditions, in the presence of nutrient medium alone (no exogenous gonadotropin), the progesterone synthetic activity of mid-luteal phase cells was significantly (P less than 0.01) greater than that of cells from late luteal phase (days 22-28) of the cycle. Moreover, progesterone production by mid-luteal phase cells was consistently stimulated (P less than 0.01) by the presence of 100 ng hCG/ml, whereas late luteal phase cells were less sensitive or unresponsive to exogenous gonadotropin. The progesterone synthetic activity of luteal cells in vitro correlated positively with both the wet weight of the excised corpus luteum (r = 0.82, P less than 0.01) and the peripheral serum progesterone concentration immediately preceding luteectomy (r = 0.66, P less than 0.01). These findings suggest that freshly isolated luteal cells reflect the functional capability of the corpus luteum in vivo. It is apparent that the age of the rhesus monkey corpus luteum of the non-fertile menstrual cycle is an important factor governing luteal cell progesterone synthetic capability and luteal cell responsiveness to gonadotropin in vitro.

Animals↗
PubMed1979

Stimulation of dopamine release into hypophysial portal blood by administration of progesterone.

To test the hypothesis that progesterone is involved in the regulation of dopamine release into hypophysial portal blood, female rats were adrenalectomized and ovariectomized at 1200 h on the day of proestrus and, immediately after the operation, injected sc with sesame oil or progesterone. Approximately 24 h later, hypophysial portal blood was collected and the plasma from this blood was analyzed for dopamine. The concentration of dopamine in portal plasma from rats given sesame oil or progesterone (50 mg) was 1.8 +/- 0.24 or 6.0 +/- 1.2 ng/ml (mean +/- SE), respectively. At the time of collection of portal blood, the progesterone concentration in arterial plasma was less than 0.8 ng/ml in rats given sesame oil and was 93 +/- 11 ng/ml in animals given progesterone. Conversely, the circulating concentrations of PRL was less (25 +/- 3 ng/ml) in animals given progesterone and higher (42 +/- 5 ng/ml) in animals given sesame oil. Twenty-four hours after the injection of progesterone (50 mg) into intact proestrous rats, the dopamine concentration in portal plasma was 5.8 +4- 1.29 ng/ml, a concentration which was significantly (P less thann 0.01) higher than that in untreated proestrous rats (1.1 +/- 0.24 ng/ml) but only slightly higher than that in untreated estrous rats (3.7 +/- 1.0 ng/ml). It is proposed 1) that progesterone administered sc can lead to an increased secretion of dopamine into hypophysial portal blood and 2) that the increased concentration of dopamine in portal plasma of intact pregnant rats relative to that of proestrous rats is, in part, a consequence of augmented progesterone secretion.

Adrenalectomy↗