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Biomedical subjects

J R Ducharme

Publications and source records attributed to J R Ducharme.

At least 19 recordsLinked to original sources
PubMed1989

Reduced pituitary volume in children with short stature: clinical and radiological correlates.

A retrospective evaluation of 80 cases of growth retardation evaluated at the Hôpital Sainte-Justine of Montreal has revealed that 20 of them (25%; 15 boys and 5 girls) had a reduction of pituitary volume as revealed by high-resolution CT scanning of the pituitary gland. Of these patients, 8 had complete growth hormone (GH) deficiency, as evaluated by arginine infusion and L-Dopa-propranolol testing and nocturnal blood sampling, and 3 had GH neurosecretory dysfunction. Five patients had combined or multiple hormonal deficiencies. A statistically significant correlation was found between nocturnal plasma GH values and pituitary volumes. From this study it can be concluded that reduced pituitary volume is a frequent finding in growth-retarded children with hypopituitarism.

Adolescent↗
PubMed1988

Cyclooxygenase products formed by primary cultures of cells from human chorion laeve: influence of steroids.

Cells were isolated from human chorion laeve obtained at term (38-40 weeks gestation) by elective caesarean section and were maintained in primary culture for 1 week in defined media supplemented with 10% fetal calf serum. The production of various cyclooxygenase products by the cultures was examined. Little or no prostaglandin (PG) F2 alpha, 6-keto-PGF1 alpha, thromboxane B2, or 13,14-dihydro-15-keto-PGF2 alpha was found. In contrast, the cells produced PGE2 which was low on day 0, increased during culture to a maximum on day 1 or 2, then declined to low levels. When cells were grown in the presence of media containing cortisol, dexamethasone, progesterone, and estradiol (at 10(-7) or 10(-9) M), the glucocorticoids (at 10(-7) and 10(-9) M), but not estrogen or progesterone, markedly inhibited the increase in PGE2 output. There was no difference in the protein content and thymidine incorporation of cells grown in the presence of glucocorticoids when compared with controls. This inhibitory effect was not sensitive to cycloheximide (1 microgram/mL) indicating protein synthesis may not be involved in the process. These studies indicate that PGE2 is the major prostaglandin formed by primary cultures of chorion laeve and that prostaglandin metabolism in the chorion is sensitive to glucocorticoid inhibition.

Cells, Cultured↗
PubMed1987

Effect of catecholamines on porcine Sertoli and Leydig cells in primary culture.

The accumulation by purified immature porcine Leydig and Sertoli cells of cyclic adenosine 3',5'-monophosphate in the presence of 1-methyl-3-isobuthylxathine was studied and their respective testosterone and 17 beta-estradiol production in response to catecholamines was assessed in vitro. These substances increased both basal and FSH-stimulated cyclic adenosine 3',5'-monophosphate accumulation in Sertoli cells. In contrast, catecholamines slightly enhanced basal cyclic adenosine 3',5'-monophosphate production but inhibited its human chorionic gonadotropin-stimulated accumulation by Leydig cells. Catecholamines had no effect on basal and stimulated testosterone release by these cells, while dopamine inhibited 17 beta-estradiol synthesis by Sertoli cells. Using various alpha- and beta-adrenergic agonists and antagonists, beta-receptors, likely of the beta 1-subtype, were shown to be present in both cell lines. Taken together these data suggest the presence of a cyclic adenosine 3',5'-monophosphate-linked adrenergic receptor in porcine Leydig and Sertoli cells, the role of which remains to be determined.

1-Methyl-3-isobutylxanthine↗
PubMed1986

Persistent effects of a marathon run on the pituitary-testicular axis.

Plasma levels of testosterone (T), LH, FSH, prolactin (PRL), cortisol (F), dehydroepiandrosterone sulfate (DHAS), noradrenaline (NA), NA sulfate (NAS), adrenaline (A) and A sulfate (AS) were measured in 7 adult males before and immediately after a marathon run as well as every morning for 5 days after the run. While plasma T levels fell significantly on the first and the second postmarathon day, those of LH rose significantly during the first 3 postrun days. Plasma PRL and F values increased significantly only at the end of the marathon. Plasma levels of NA and NAS rose significantly at the end of the run and again on days 2 and 5 postmarathon, respectively. A similar pattern was observed for A and AS except for the second peak of free A. These results show that a strenuous physical exercise leads to a persistent relative insensitivity to LH of the testicular T biosynthetic machinery, while the feedback mechanisms operating at the hypothalamic-pituitary level are normal. Furthermore, they suggest that catecholamines may be responsible for the prolonged inhibitory effect of stress on T biosynthesis.

Adult↗
PubMed1986

Inhibition of prolactin release and blockade of adenohypophyseal cell cyclic AMP accumulation are two dissociable effects of dopaminergic and non-dopaminergic drugs.

The secretion of PRL by the anterior pituitary gland is under a tonic inhibitory control exerted by dopamine (DA). However, the mechanism(s) involved in the inhibition of PRL secretion is not clearly defined. Several recently published papers supported the hypothesis that DA inhibits the release of PRL through blockade of the pituitary adenylate cyclase-cyclic AMP system. We have recently demonstrated that sodium ions are essential for dopaminergic inhibitory action on PRL secretion. The present paper reports the effects, in the presence or in the absence of Na+, of either DA, bromocriptine, apomorphine or 2 anticalmodulin drugs, penfluridol and W-7, on cyclic AMP accumulation by rat adenohypophyseal cells in primary culture. Studies with dopaminergic agonists show that in the presence of Na+ inhibition of both PRL and cyclic AMP is obtained at 15 and 30 min, while in the absence of the ion a dissociation exists between the inhibition of PRL release which is completely abolished, and that of cyclic AMP content which is still present. Dose-response studies done in the presence of Na+ show the existence of a good correlation between hormone and nucleotide effects of dopaminergic agonists while, in the absence of Na+, a dissociation is observed between the inhibition of PRL release, which is completely suppressed, and that of cyclic AMP accumulation which is slightly or not at all decreased. The inhibitory effects of penfluridol after 15 and 30 min of incubation were not suppressed by Na+ removal, although its hormonal actions were slightly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

Isolation, purification and culture of Sertoli cells from immature piglet testes.

Several studies suggest a role of Sertoli cells in the control of Leydig cell steroidogenesis. In order to verify this hypothesis, we have developed a system for the purification of pig Sertoli cells. These cells were then characterized by their morphological appearance in light and electron microscopy, their ability to bind [125I]follicle stimulating hormone (FSH) and their functional capacity as evaluated by adenosine 3',5' monophosphate (cAMP) accumulation and lactate production when in primary culture under basal and FSH-stimulated conditions. Crude Sertoli cell suspensions from immature porcine testes were fractionated on discontinuous Percoll gradients (densities 1.025, 1.039, 1.055, 1.080 g/ml). Highly purified Sertoli cells were contained in the second band (d: 1.039) generated on the gradient. These cells demonstrated morphological and functional integrity as evidenced by binding specifically [125I] FSH and by responding to FSH stimulation (by an increased production of cAMP and lactate after 3 days in primary culture), but not to human chorionic gonadotrophin (hCG). This preparation represents a useful model for the study of Sertoli cell functions and their interation with Leydig cells in the regulation of testicular steroidogenesis.

Animals↗
PubMed1984

Role of catecholamines in the inhibitory effect of immobilization stress on testosterone secretion in rats.

Immobilization stress applied for 6 h induced, in adult male rats, a rise of epinephrine (E) and norepinephrine (NE) plasma levels and a decrease of baseline plasma testosterone (T) values and of human chorionic gonadotropin (hCG)-induced T response. Treatment of the animals for 5 weeks with guanethidine (G), a sympathetic neuron toxic agent, significantly decreased E and NE responses to stress and partly antagonized the inhibitory effects exerted by immobilization on T biosynthesis. Adrenalectomy totally suppressed circulating E and reduced the stress-induced NE increase while partly antagonizing the inhibitory effects exerted on T biosynthesis. Combined G and adrenalectomy treatments totally suppressed plasma E and NE, and completely blocked the effects of immobilization on T levels. Treatment of the animals with the alpha 1-adrenergic blocker, prazosin, and the beta 1-adrenergic blocker, metoprolol, did not modify the effects of stress on T biosynthesis. Treatment with propranolol or with butoxamine, a nonspecific beta- and a specific beta 2-adrenergic receptor blocker, respectively, antagonized the testicular hyposensitivity to hCG induced by stress. Stress- or treatment-induced changes of plasma luteinizing hormone (LH) and hCG levels were not consistently correlated with plasma T modifications. These findings suggest that at least part of the inhibitory effects of immobilization stress on T biosynthesis is exerted by catecholamines through a beta 2-adrenergic receptor.

Adrenal Glands↗
PubMed1984

Effect of glucocorticoids on testosterone production by porcine Leydig cells in primary culture.

For this study, purified immature porcine Leydig cells in primary culture were used. After 2 days of culture, the cells were incubated with dexamethasone (5 X 10(-9), 1 X 10(-7) M) for various periods of time (3-45 h). The media were discarded and treatment was repeated with or without the addition of human chorionic gonadotropin (HCG, 10 mIU/mL) for 3 h. Dexamethasone (10(-7) M) decreased testosterone production of HCG-treated cells (up to 40%) in a time-dependent fashion while the lower dose was ineffective. The effect of varying doses (10(-8) and 10(-6) M) of natural glucocorticoids (corticosterone, cortisol) or synthetic glucocorticoids (triamcinolone, triamcinolone acetonide, betamethasone, dexamethasone) and that of a synthetic progestin (R-5020) on cultured Leydig cells was also studied. After 18 h of preincubation, the various synthetic but not the natural steroids nor R-5020, were able to decrease testosterone production of control and HCG-treated cells by 20-40%. Of a number of other hormonal and nonhormonal substances studied at concentrations of 10(-9)-10(-5) M, only lysine8-vasopressin at a concentration of 10(-6) M was able to inhibit testosterone production by these cells. These results indicate that dexamethasone and other synthetic glucocorticoids, and to a lesser degree lysine8-vasopressin, may exert a direct inhibitory effect on testosterone production by purified porcine immature Leydig cells in vitro.

Animals↗
PubMed1984

The 3 beta-hydroxysteroid dehydrogenase activity of cultured porcine Leydig cells in primary culture.

Previous studies have shown that there is a spontaneous progressive increase in human chorionic gonadotropin (HCG)-stimulated testosterone (T) production by immature porcine Leydig cells during primary culture for 3 days, whereas basal T production is unaltered. Preliminary data indicated that during this time, there was an increase in the activity of the 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD). The purpose of the present study was to further characterize this increase. 3 beta-HSD was assayed by measuring the conversion of tritiated dehydroepiandrosterone (DHEA) to androstenedione in the presence of NAD+. A ninefold increase in activity occurred between days 1 and 2 and only twofold between days 2 and 3. A 5- to 20-fold increase of the apparent maximum velocity of the enzyme was observed after 3 days of culture while the apparent Km remained unchanged. Cycloheximide treatment (150 ng/mL) completely abolished this spontaneous increase in enzyme activity. In parallel experiments, the stimulatory effect of HCG on T and DHEA production was inhibited by cycloheximide treatment by 90% and 60%, respectively, whereas basal T production was not affected. These results suggest that the spontaneous increase of 3 beta-HSD activity in primary cultures of porcine Leydig cells is secondary to de novo protein synthesis and that this phenomenon may be partially responsible for the increased responsiveness of these cells to HCG during the culture period.

3-Hydroxysteroid Dehydrogenases↗
PubMed1984

Sodium ions: their role and mechanism of action in the control of prolactin release.

The secretion of PRL by the pituitary gland is under a tonic inhibitory control exerted by dopamine. However, the mechanisms involved in this inhibition remain to be completely defined. We have investigated the effects of sodium removal in the incubation medium on baseline PRL, on the inhibitory effects exerted by bromocriptine, haloperidol and cobalt, and on the stimulatory action of TRH and vasoactive intestinal polypeptide (VIP) on PRL release by enzymatically dispersed rat anterior pituitary cells in primary culture. The effects of ouabain, tetrodotoxin, and veratridine on baseline PRL release and on the inhibitory effects of dopaminergic agents were also investigated. Basal PRL release was slightly but significantly reduced by replacing sodium by choline in the incubation medium and was almost completely suppressed when isoosmolar concentrations of glucose were substituted for sodium. On the other hand, ouabain slightly but significantly increased basal release of the hormone. In the absence of sodium, the dose-dependent inhibitory effect of bromocriptine was greatly reduced. Of two antidopaminergic drugs, haloperidol and l-sulpiride, only the first inhibited the release of PRL at high doses (10(-5) - 10(-4) M) in the presence of sodium but became stimulatory at 10(-4) M in the absence of the ion. Ouabain, tetrodotoxin, and veratridine failed to significantly modify the inhibitory effects of either dopamine or bromocriptine. The dose-dependent inhibitory effects of cobalt and the releasing actions of TRH and VIP were not significantly influence by sodium removal from the incubation medium, although VIP appeared to be active at a lower concentration in the absence of the ion. These data indicate that, although the presence of a normal ionic charge in the incubation medium is essential for the baseline secretion of PRL, sodium ions specifically play only a minor role in a phenomenon which is essentially Ca2+-dependent. They also clearly show that sodium intervenes in dopaminergic agonist and antagonist inhibition of PRL release through a mechanism which appears independent of either dopaminergic receptor, Ca2+ or Na+ channel, or Na+/K+ pump. It is hypothesized that a normal intracellular sodium concentration is essential for dopaminergic agonist or antagonist inhibitory action.

Animals↗
PubMed1984

Role of arginine-vasopressin (AVP) in stress-induced inhibition of testicular steroidogenesis in normal and in AVP-deficient rats.

It has been recently demonstrated that immobilization stress induces in rats a state of testicular desensitization to gonadotropins as well as a post-cAMP blockade of testosterone (T) biosynthesis. Since arginine-vasopressin (AVP) has recently been found to antagonize in rats the in vitro T-releasing effect of human CG, with this work we have verified whether AVP might be involved in stress-induced inhibition of T biosynthesis. In Sprague-Dawley and Long-Evans adult male rats chronically cannulated in the jugular vein, a small but statistically significant rise of plasma AVP levels was observed after 2 h of immobilization stress. The iv infusion of AVP (1 micrograms/kg/h) to chronically cannulated rats induced a fall of plasma T levels. A dose-dependent inhibition of plasma T values was also observed 3 h after ip administration of AVP (1, 5, 25 micrograms/kg) in animals killed by decapitation. An antagonist of AVP pressor activity [1-(beta-mercapto-beta 1 beta-cyclopentamethylenepropionic acid), 2-(O-methyl)tyrosine] AVP, antagonized, when injected ip at a dose of 30 micrograms/kg, the T-inhibitory effects of 3 h of immobilization stress. No consistent changes in plasma LH levels were observed in these experiments. To further evaluate the role of AVP in stress-induced T inhibition, AVP-deficient Brattleboro rats were submitted to 2 or 3 h of immobilization stress concomitantly with rats of the original Long-Evans strain. After 2 h and even more after 3 h of stress, plasma T levels fell in Long-Evans rats together with basal and human CG- or cAMP-stimulated T production by Percoll purified Leydig cells. In Brattleboro rats, 2 h of stress had no effects on plasma T levels nor in vitro basal or stimulated T production, whereas 3 h of immobilization were as effective as in Long-Evans animals. These results suggest, therefore, that at least part of T inhibitory effects of immobilization, those occurring during the first 2 h of stress, are due to an AVP-induced, post-cAMP blockade of T biosynthesis. Since plasma corticosterone, during 2 h of stress, rose to similar, albeit smaller, levels in Brattleboro rats as compared to those in Long-Evans animals, this glucocorticoid does not seem to be involved in the testicular effects of stress.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1983

Maturation of the hypothalamic--pituitary--gonadal axis in the male lamb: a review.

We have studied the activity of the hypothalamic--pituitary--gonadal (HPG) axis in the male ovine fetus and newborn lamb. Circulating levels of gonadotropins, prolactin, cortisol (F), testosterone (T), dehydroepiandrosterone sulfate and delta 4androstenedione (delta 4A) were measured in fetal plasma in the third trimester of gestation and the testicular response to hCG was studied in ovine fetuses at 95 - 141 days. Ultradian variations of LH, FSH and testosterone and the testicular response to hCG also were assessed from 1 to 28 days postnatally. The data indicate that (1) fetal plasma LH, FSH, delta 4A and T levels are low from 95 days of gestation to term, while F levels increase in the last 10 days. Postnatally, F decreases rapidly. Spontaneous T peaks may occur as early as 36 hr of life. (2) Spontaneous LH and concomitant or subsequent T secretory peaks are observed by 3 days of age. (3) hCG can induce an increase in T production by interstitial cells in vitro and can increase the T testicular content and its release in the plasma from 95 days of intrauterine life. Desensitization to hCG also can be observed throughout the last trimester of gestation. We conclude that the HPG axis of the male lamb is active ty 36 - 72 hr of postnatal life and that the steroidogenic capacity of the ovine testis is developed several weeks prenatally. Consequently, the relative quiescence of the axis prenatally and in the first 24 hr of life seems to result from relatively low LH secretion and release, related to an undefined endogenous control, together with decreased Leydig cell sensitivity and relatively low enzyme activity limiting T release.

Animals↗
PubMed1983

Studies with purified immature porcine Leydig cells in primary culture.

The steroidogenic capacity of purified immature porcine Leydig cells in culture was studied over several days. The cells were obtained by fractionating crude testicular interstitial cell suspensions on a discontinuous Percoll gradient (d = 1.037, 1.042, 1.052, 1.098 g/ml), and characterized by specific binding of 125I-human chorionic gonadotropin (hCG), testosterone (T) and cyclic adenosine 3':5'-monophosphate (cAMP) production in response to hCG, and the enzymatic determination of delta 5-3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) activity. The Leydig cells were recovered in a density band between 1.052-1.068 g/ml and grown in a chemically defined medium (Mather et al., 1981). In the absence of hCG, T production was low throughout the 6 days of culture. However, in response to hCG (10 mIU/ml), the cultured Leydig cells showed a progressive increase in T synthesis, which reached a maximum at Days 3-4. 8-Br-cAMP (1 mM) induced a comparable rise in T production to that obtained with hCG throughout the culture period. In contrast, 8-Br-cAMP induced a near maximal increase in dehydroepiandrosterone (DHEA) production from Day 1. This paper demonstrates that purified immature porcine Leydig cells in primary culture are a valuable model to study the ontogeny of Leydig cell function.

3-Hydroxysteroid Dehydrogenases↗
PubMed1983

Postreceptorial refractoriness of prolactin release mechanisms.

While a first injection of the antidopaminergic benzamide drug, sulpiride, induced a large rise in plasma prolactin (PRL) levels in chronically cannulated adult male rats, a second injection given 2 h later was totally inactive although the pituitary content of the hormone was still 76% of the initial value. When the second injection was given 8 h after the first it was slightly effective, but when administered 24 h later it was as effective as the first. The second of two consecutive injections of haloperidol given at 2-h intervals, or an injection of morphine given 2 h after sulpiride, were incapable of inducing a release of PRL. Two hours after an injection of sulpiride, a 30-min period of immobilization stress induced a significant rise in plasma PRL levels. A significant rise in plasma PRL levels was also observed when larger doses of sulpiride were given 2 h after a first injection of the drug. Apomorphine was at least as effective an inhibitor of PRL secretion when given 2 h after sulpiride than when injected after saline. In vitro studies of dopaminergic binding sites revealed the presence, in pituitary glands of sulpiride-treated rats, of receptors not modified by the drug. These data suggest that the only plausible explanation for the ineffectiveness of the second of two consecutive injections of sulpiride is the development of a state of refractoriness of the mechanisms that subserve the release of PRL induced by suppression of the inhibitory dopaminergic tonus.

Animals↗
PubMed1983

Testicular responsiveness to hCG of the ovine fetus in the last third of gestation.

The in vivo and in vitro testicular responsiveness to hCG of hemicastrated lamb fetuses 95-99, 110-118 and 130-141 days of gestational age was studied. Basal plasma testosterone (T) levels were similar at all ages (less than 0.25 ng/ml), while the mean testicular concentrations of dehydroepiandrosterone sulfate (DHA-S), 17 alpha-hydroxyprogesterone (17-OHP) and T were higher in 95- to 99-day-fold fetuses. Plasma T levels and the concentration of T, DHA-S, 17-OHP, androstenedione (A) and cyclic adenosine 3'5'-monophosphate (cAMP) were increased by hCG in the hemicastrated animal at all ages. cAMP and T production by enriched preparations of dispersed interstitial cells from control testes was increased by hCG in all groups. In fetuses pretreated with hCG in vivo the addition of hCG in vitro failed to modify cAMP and T production. 100 micrograms of LHRH to a 130-day-old fetus increased plasma LH and T levels. From these experiments, it is suggested that the low plasma LH and T levels found throughout the last trimester of fetal life reflect a relative lack of endogenous LHRH synthesis and/or release, rather than reduced testicular steroidogenic capacity.

17-alpha-Hydroxyprogesterone↗
PubMed1982

Pubertal development: normal, precocious and delayed.

The present concepts on the neuroendocrine mechanisms which trigger pubertal development and modulate the progression towards sexual maturity have been reviewed. Essentially, puberty is presented as a continuum, the programming of which is initiated prenatally and which ends in adult life when all hormonal secretions become autoregulated. This continuum is dependent on a delicate equilibrium between CNS neurohormones (GnRH), neurotransmitters (biogenic amines), pituitary gonadotrophin (FSH, LH) secretion and the end-organ response (testis or ovary) through the activation of specific membrane receptors. The gonadal sex steroids (T, OE2) will activate specific cytoplasmic and nuclear receptors of target tissues and exert their biological action. Initially, the activity of the HPGA is manifested by nocturnal LH peaks, followed by increased gonadal secretion of T or OE2. Extremely sensitive to negative feedback by circulating androgen and/or oestrogen in prepuberty, an hypothalamic regulatory system called the gonadostat increases its threshold of sensitivity and eventually becomes autoregulated at a higher feedback level. Progressively, the hypothalamus becomes sensitive to positive feedback action of gonadal hormones, this phenomenon being important for the onset of ovulation. It is likely also that adrenal androgens play a permissive and supportive role in the onset and progression of pubertal development. Finally, full maturity is reached, with final adult height through fusion of the epiphysis, and fertility is achieved. The clinical manifestations of each developmental stage of puberty are described and abnormalities of sexual development reviewed. While over 90 per cent of cases of precocious pubertal development are idiopathic in girls, a space-occupying lesion in the hypothalamic-pituitary region is frequent in boys. Dissociated pubertal signs (premature adrenarche, pubarche, thelarche, menarche) are discussed, together with diagnosis and treatment of precocious puberty, whether it is idiopathic or occurring independently of the activation of the HPGA. In addition to delay of puberty on a constitutional basis, or related to chronic endocrine or non-endocrine diseases, the main clinical entities with gonadal insufficiency, primary (hypergonadotrophic) or secondary (hypogonadotrophic), are reviewed in boys and girls and their investigation and treatment discussed.

Adolescent↗
PubMed1982

Stress-induced testicular hyposensitivity to gonadotropin in rats. Role of the pituitary gland.

The time course of stress-induced testicular hyposensitivity to gonadotropins was studied in hypophysectomized or naloxone-treated rats exposed to various periods of immobilization. Blood was collected from a chronically indwelling intra-atrial catheter every hour for luteinizing hormone (LH) and testosterone (T) measurement. Eight hours of immobilization completely suppressed T secretion without significant effect on LH. Human chorionic gonadotropin (hCG, 5 IU/rat, i.m.) induced a marked increase in plasma T levels in normal control groups 3 h post-injection while in immobilized rats the response was completely abolished, even after only 30 min of stress. In hypophysectomized rats, as expected, plasma T levels were undetectable, but, contrary to results obtained in normal animals, hCG induced a similar increase of plasma T levels both in control and stressed rats. Immobilization stress failed to inhibit plasma T values in hypophysectomized rats pretreated for 4 days with human menopausal gonadotropin (hMG) + hCG, while it did so in similarly treated normal animals. Naloxone induced a rise of plasma LH and T levels in control rats, but did not antagonize the stress-induced fall of plasma T concentration. In all groups, steroid testicular content mimicked variations of plasma T values. In particular, in stressed animals the lack of accumulation of testicular 17-hydroxyprogesterone probably reflected a normal activity of 17-20 lyase. These results indicate that stress induces very rapidly a state of Leydig cell hyposensitivity to gonadotropins and a blockade of T biosynthesis. The causal relationship between the two effects is presently not clear but these events seem to be due to stress-induced release of an inhibitory factor of pituitary origin other that endorphin.

Adrenocorticotropic Hormone↗