Adrenal glands of mouse and rat do not synthesize androgens.

Human adrenal glands produce considerable amounts of the C-19 steroids dehydroepiandrosterone (DHEA) and androstenedione. To investigate the capability of rodent adrenals to produce these steroids, cell suspensions of mouse and rat adrenal glands were incubated in the absence and presence of adrenocorticotropic hormone (ACTH). Corticosterone levels in the incubation medium increased dramatically in the presence of ACTH, but no significant amounts of 17-hydroxyprogesterone or androstenedione could be detected. This indicates that the adrenals of rat and mouse lack the enzyme 17 alpha-hydroxylase. Absence of plasma cortisol in the presence of high levels of corticosterone confirmed these data. Plasma levels of androstenedione were significantly decreased in castrated male rats as compared to levels observed in intact males, showing the contribution of the testes to the plasma content of androstenedione. Very low levels of androstenedione were observed in female, male and castrated male mice. Plasma concentrations of DHEA were not detectable in intact and castrated male mice and rats. It is concluded that rat and mouse lack the enzyme necessary to synthesize adrenal C-19 steroids and that the adrenals in these animals, therefore, do not contribute to plasma levels of androstenedione and DHEA.     

Evidence for sex-dependent anabolic response to androgenic steroids mediated by muscle glucocorticoid receptors in the rat

The muscle anabolic/anti-catabolic activity of the androgenic steroids testosterone and trenbolone was studied in rats to investigate whether such steroids act as agonists via muscle androgen receptors, or as antagonists that oppose the catabolic effects of endogenous glucocorticoids via their interaction with muscle glucocorticoid receptors. For comparison, the effects of the potent glucocorticoid antagonist RU486 were also examined. The parameters measured included growth rate, muscle weight, serum growth hormone and corticosterone levels, and receptor binding parameters in muscle cytosol. Females responded better than males to anabolic treatment with the androgenic steroids. Ovariectomy or adrenalectomy abolished this response. Neither the sex difference nor the requirement for ovaries or adrenals could be explained in terms of muscle receptor parameters or serum growth hormone levels. The muscle anabolic activity of androgenic steroids was restored when castrated males were treated with oestradiol and when adrenalectomized females were treated with corticosterone. RU486 also prevented the catabolic/anti-anabolic activity of exogenous corticosterone in adrenalectomized rats. Testosterone and RU486 behaved as anti-glucocorticoids in vivo since they inhibited glucocorticoid-induced liver tyrosine aminotransferase activity. The results suggest that anabolic steroids can act via muscle glucocorticoid receptors, thereby antagonizing the catabolic activity of endogenous glucocorticoids, rather than via muscle androgen receptors.     

Ultrastructural evidence for endogenous testosterone immunoreactivity in the pituitary gland of the rat

Summary Several attempts have been made to localize steroids by means of immunocytological techniques. However, these methods were found inadequate for detecting steroids bound to their receptors. To localize endogenous testosterone (T) in its target cells at the ultrastructural level, an immunocytological technique was performed on ultrathin sections obtained by cryo-ultramicrotomy. T was detected in the pituitary glands obtained from intact male or female rats and castrated rats, but not in castrated + adrenalectomized rats. Animals were also injected either with testosterone, with other steroids (estradiol, progesterone, corticosterone) or with an androgen antagonist (cyproterone acetate). In addition, some ultrathin sections were preincubated either with phosphate buffers of various pH, corticosterone, cyproterone acetate solution, or with T solution. The content of T in the pituitary before and after fixation was measured by radioimmunoassay; it decreased after fixation. T immunoreactivity was localized in the gonadotropic cells only, both in the male and female rats. At the subcellular level, the immunoreactivity was detected in the cytoplasmic matrix and in the nucleus. Immunoreactive T disappeared 1) in rats after castration+adrenalectomy; by means of radioimmunoassay no T was measured in these pituitary glands; 2) in rats injected with 25 (g/rat of cyproterone acetate; 3) after preincubation of pituitary sections on a drop of cyproterone acetate (1 × 10^-6 M). The immunocytological reaction was not modified when the rats were injected with estradiol, progesterone or corticosterone (1 mg/rat), or after preincubation of the sections with corticosterone (1 × 10^-3 M), or a buffer solution at pH 7.6. Lower or higher pH values led to a strong decrease in the immunoreactivity. After injection of T (15 g/rat) the immunocytological reaction was more abundant in the nucleus and less in the cytoplasm. The immunoreactivity was again observed when the sections were preincubated with cyproterone acetate solution and then with T solution. These data suggest that T can be detected by means of immunocytochemistry. It is probably bound to a specific binding site.This work was presented in part at the VI^th International Congress on Hormonal Steroids, Jerusalem, 1982     

Sex-differences in adrenocortical responsiveness during development in rats

It is known that the stress hyporesponsive period (SHRP), which seems to be related to an immature hypothalamo-pituitary-adrenal (HPA) regulatory system, occurs during the first 2 weeks after birth in rats. In the present study, we investigated the effects of sex-steroid hormones on adrenocortical responsiveness to adrenocorticotropic hormone (ACTH) in neonatal rats. The levels of cyclic adenosine 3',5'-monophosphate (cAMP), corticosterone, and adenylate cyclase activity increased with the dose of ACTH in adrenal cells of males and females in vitro. The ACTH responsiveness in adrenal cells increased with age (7-35 days of age), that is, the loss in responsiveness to ACTH just after birth began to recover in 14-35-day-old rats, but the responsiveness in 14-day-old rats was attenuated in males compared with females. Although castration markedly augmented the responsiveness in male rats, testosterone-replacement in the castrated male rats inhibited the enhancement. Furthermore, the responsiveness in 14-day-intact female rats was suppressed by treatment with testosterone. Expression levels of ACTH receptor mRNA in adrenals increased with age in the female rat, but not in the male. Castration enhanced the level of ACTH receptor mRNA to three-fold of that in intact male rats at 14 days of age, but replacement treatment with testosterone in castrated male rats lowered the elevated levels. Testicular androgens are thought to evoke a gender-specific response in neonates, and the temporal decrease of adrenal ACTH-responsiveness might be due to the topically immature adrenal system as well as the central nervous system in mammals.     

The hormonal response of female European Stonechats to a territorial intrusion: the role of the male partner

In many bird species, the female participates in defending a pair's breeding territory, however, the endocrine control mechanism of female aggressive behavior is largely unknown. The general statement that androgens are involved in the regulation of aggressive behavior is based on studies conducted only in males. Here, we tested whether paired female stonechats show a hormonal response to a simulated male territorial intruder. Since in males of territorial bird species androgen levels usually increase following a male-male encounter, we measured androgen-levels before and after a simulated male intrusion. In addition, we measured estradiol, the main gonadal hormone in females, and corticosterone, a stress hormone. The results show that a male intruder does not affect any of the measured hormones in females. In a second experiment, we also tested whether the endocrine state of the male partner affects the hormonal response of females to a male intruder by comparing the hormonal response of females paired with pharmacologically castrated males and females paired with control males. Females paired with pharmacologically castrated males had lower corticosterone levels both before and after the intrusion than females paired with control males. Additionally, in both groups, female corticosterone levels were increased following a male intrusion. We suggest that the differences found between females paired with pharmacologically castrated males and females paired with control males are due to differences in intra-pair interactions.     

Regulation of 11 beta-hydroxysteroid dehydrogenase enzymes in the rat kidney by estradiol

The 11beta-hydroxysteroid dehydrogenase (11betaHSD) type 1 (11betaHSD1) enzyme is an NADP+-dependent oxidoreductase, usually reductase, of major glucocorticoids. The NAD+-dependent type 2 (11betaHSD2) enzyme is an oxidase that inactivates cortisol and corticosterone, conferring extrinsic specificity of the mineralocorticoid receptor for aldosterone. We reported that addition of a reducing agent to renal homogenates results in the monomerization of 11betaHSD2 dimers and a significant increase in NAD+-dependent corticosterone conversion. Estrogenic effects on expression, dimerization, and activity of the kidney 11betaHSD1 and -2 enzymes are described herein. Renal 11betaHSD1 mRNA and protein expressions were decreased to very low levels by estradiol (E2) treatment of both intact and castrated male rats; testosterone had no effect. NADP+-dependent enzymatic activity of renal homogenates from E2-treated rats measured under nonreducing conditions was less than that of homogenates from intact animals. Addition of 10 mM DTT to aliquots from these same homogenates abrogated the difference in NADP+-dependent activity between E2-treated and control rats. In contrast, 11betaHSD2 mRNA and protein expressions were significantly increased by E2 treatment. There was a marked increase in the number of juxtamedullary proximal tubules stained by the antibody against 11betaHSD2 after the administration of E2. Notwithstanding, neither the total corticosterone and 11-dehydrocorticosterone excreted in the urine nor their ratio differed between E2- and vehicle-treated rats. NAD+-dependent enzymatic activity in the absence or presence of a reducing agent demonstrated that the increase in 11betaHSD2 protein was not associated with an increase in in vitro activity unless the dimers were reduced to monomers.     

Changes in masculine sexual behavior, corticosterone and testosterone in response to acute and chronic stress in male rats

Chronic exposure to stressors increases HPA axis activity and concomitantly reduces HPG axis activity. This antagonistic relationship between both these axes has been proposed to underlie the inhibition of reproductive function due to stress. Sexual behavior in males may be the most vulnerable aspect of male reproduction to acute and chronic stress and it has been suggested that alterations in sexual behavior during stress are due to the antagonistic relationship between testosterone and corticosteroids. However, only in a few studies has a correlation between the levels of testosterone and corticosterone, and sexual behavior been made. In this study, we evaluated the effects of different stressors, applied both acute and chronically, on masculine sexual behavior and whether or not these effects on sexual behavior are accompanied by changes in plasma levels of corticosterone and testosterone. Additionally, we evaluated the effect of testosterone treatment on the effects of stress on sexual behavior. Sexually experienced male rats were exposed to one of the following stressors: immobilization (IMB), electric foot shocks (EFS) or immersion in cold water (ICW). Sexual behavior and plasma levels of testosterone and corticosterone were assessed on days 1, 5, 10, 15, and 20 of stress. In a second experiment, males were castrated, treated with 3 different doses of testosterone propionate (TP) and exposed to ICW for 20 consecutive days. Sexual behavior was assessed on days 1, 5, 10, 15, and 20 and steroids were evaluated on day 20. Parameters of masculine sexual behavior were modified depending on the characteristics of each stressor. Mount, intromission and ejaculation latencies increased significantly, the number of mounts increased, and ejaculations decreased significantly in males exposed to EFS and to ICW but not in males exposed to IMB. Associated with these effects, testosterone decreased in the EFS and ICW groups on days 1, 15, and 20. However, corticosterone increased only in males exposed to ICW. In castrated males, TP treatment failed to block the effects of stress by ICW on sexual behavior and corticosterone. These results indicate that the effects of stress on sexual behavior depend on the characteristics of each stressor, and these effects, as well as the decrease in testosterone are not necessarily associated with the increase in corticosterone. The fact that testosterone treatment did not prevent the effects of stress on sexual behavior suggests that other mediators could be involved in the alterations of sexual behavior caused by stress.     

Influence of testosterone on the development of the ischiocavernosus muscle of the rat

The mean area of the neuromuscular endplates and the acetylcholinesterase (AChE) activity at the myotendinous junction of the ischiocavernosus muscle were studied in normal, castrated and testosterone-treated castrated Wistar rats by the Koelle method. The mean endplate area was found to be smaller in castrated rats, compared to normal ones (p less than 0.001), while testosterone treatment restored its normal size (0.8 greater than p greater than 0.7). The terminal AChE activity in castrated rats was as strong and spread as in juvenile ones, while it was almost absent in normal and in testosterone-treated castrated rats. The same parameters were examined in the tibialis anterior muscle of the same rats, chosen as a specimen of 'nonhormone-dependent' muscle, without finding any difference among the single groups.     

The effects of dichloromethylene biphosphonate on osteoporotic femora of adult castrate male rats

In a previous study we reported that castration of adult male rats resulted in femoral osteoporosis 4 months later. The present study tested the effects of dichloromethylene biphosphonate (Cl2MBP, formerly Cl2MDP), a bone resorption inhibitor, on the development of osteoporosis in femora of adult castrated male rats. One-year-old male Holtzman rats were assigned to three groups: sham-operated controls; castrated-no treatment; castrated + Cl2MBP injections 3 times/week. The animals were sacrificed 4 months later. Femora from untreated castrated rats were osteoporotic, confirming our earlier study. Femora from Cl2MBP-treated castrates did not differ from those of controls and were significantly denser and more robust than those of untreated castrated rats. The results indicated that Cl2MBP treatment started immediately after castration prevented the development of femoral osteoporosis in adult castrated male rats.     

Sex differences in adrenal function in the lizard Cnemidophorus sexlineatus: II. Responses to acute stress in the laboratory.

Circulating concentrations of plasma corticosterone and gonadal steroids were measured in intact and gonadectomized male and female lizards (Cnemidophorus sexlineatus) following acute stress (handling) in the laboratory. There was a significant increase in plasma corticosterone after stress. Whereas intact females exhibited greater concentrations of corticosterone relative to intact males, ovariectomized females exhibited lower concentrations of corticosterone relative to castrated males. In addition to sex differences in corticosterone responses to gonadectomy, progesterone was elevated by stress in both intact and ovariectomized females but not in males. Corticosterone adjusted for castration and handling in males was negatively correlated with the plasma androgen level. The adrenal responsiveness of males to acute stress may be attenuated by androgens presumably secreted by the testis. Not only does adrenal function influence reproduction, but adrenal responses differ between males and females, and appear to be influenced by the gonadal axis. The sex differences in adrenal responses to stress likely reflect different reproductive strategies and nutritional requirements of males and females during the breeding season.     

Role of the pituitary-adrenocortical axis in the control of agonistic behaviour after single and repeated footshock in castrated male mice

Two experiments were conducted to examine the role of the pituitary-adrenocortical axis in the mediation of the effects of single and repeated electric footshock on subsequent agonistic responding in castrated male mice. It was found that (1) preventing corticosterone responses to shock occludes the facilitatory effects of single shock on both aggressive and submissive behaviour and occludes the additional increases in submissive behaviour which normally occur after repeated shock, and (2) blocking pituitary release of ACTH by dexamethasone treatment restores aggressive behaviour after repeated shock, independently of the initial levels of corticosterone and testosterone. These findings suggest that (1) increases in aggressive and submissive behaviour in response to single shock depend on shock-induced increases in corticosterone levels; (2) further increases in submissive behaviour in response to repeated shock require further increases in the corticosterone levels; and (3) inhibition of aggressive behaviour after shock repetition appears to depend on increases in ACTH levels, and occurs independently of the initial corticosterone and testosterone levels.     

Influences de la castration et du propionate de testosterone sur le comportement des rats conditionnes par paires

Four groups of 10 male rats (Group A: normal rats, Group B: castrated rats, Group C: castrated rats + 1 mg P.T./day, Group D: castrated rats + 1 dose of 50 mg/kg of P.T. cyclohexane) were avoidance conditioned during nine sessions of 50 trials. They were conditioned individually during sessions 4, 5 and 6 and by pairs during sessions 1, 2, 3, 7, 8 and 9. During these last sessions, all groups presented a low level of acquisition and aggressive behaviour. These phenomena were worsened in the castrated rats whose performances stayed low even when they were conditioned individually. On the other hand, the frequency of their aggressive behaviour was often higher than that of the other groups. The injection of P.T. cyclo-hexane improves the performance of the castrated animals but does not entirely compensate for the differences between control and experimental rats.     

Synthesis and androgen effects of 7 alpha,17 beta-dihydroxy-5 alpha-androstan-3-one, 5 alpha-androstan-3 alpha,7 alpha,17 beta-triol and 5 alpha-androstane-3 beta,7 alpha,17 beta-triol

The steroids 7 alpha,17 beta-dihydroxy-5 alpha-androstan-3-one (7 alpha-hydroxy-Dht), 5 alpha-androstan-3 alpha,7 alpha,17 beta-triol (7 alpha-hydroxy-3 alpha-A'DIOL) and 5 alpha-androstane-3 beta,7 alpha,17 beta-triol (7 alpha-hydroxy-3 beta-A'DIOL) have been synthetized from 7 alpha,17 beta-dihydroxy-4-androsten-3-one (7 alpha-hydroxy-testosterone). The effect of administering 7 alpha-hydroxy-Dht, 7 alpha-hydroxy-3 alpha-A'DIOL or 7 alpha-hydroxy-3 beta-A'DIOL on serum levels of LH, FSH and on ventral prostate and seminal vesicle weight were investigated in gonadectomized adult male rats. Each steroid was administered for seven days in a dose of 300 micrograms per day. No suppression of serum LH or FSH levels was recorded following injections of these 7 alpha-hydroxylated steroids to castrated rats, compared to castrated control rats receiving vehicle only. Administration of 7 alpha-hydroxy-Dht or 7 alpha-hydroxy-3 alpha-A'DIOL to castrated mature rats could maintain ventral prostate and seminal vesicle weights above that of castrated control rats. Administration of 7 alpha-hydroxy-3 beta-A'DIOL to castrated mature rats resulted in ventral prostate weights slightly above castrate control levels, while seminal vesicle weight in such rats were in the same range as castrated control rats. Intraperitoneal administration of testosterone or of 5 alpha-androstane-3 beta,17 beta-diol (3 beta-A'DIOL) to castrated rats maintained activity of the androgen dependent isoenzyme of acid phosphatase in the ventral prostate; 7 alpha-hydroxy-testosterone or 7 alpha-hydroxy-3 beta-A'DIOL showed, however, no effect on this enzymic activity.     

Testosterone and corticosterone co-regulate messenger RNA coding for secretory proteins in the epididymis of the lizard (Lacerta vivipara)

The hormonal requirements for the regulation of Lv132 mRNA coding for two proteins secreted by the principal cells of the lizard epididymis were examined by organotypic culture experiments. Testosterone, R1881 and corticosterone induced accumulation of Lv132 mRNA in explants from lizards castrated immediately after differentiation of the principal cells. The induction by testosterone was inhibited by the addition of cyproterone acetate. Progesterone and oestradiol alone or in presence of testosterone were ineffective. Unlike the induction by testosterone, the effect of corticosterone did not require binding on the androgen receptor as shown by competition binding studies. Corticosterone failed to induce gene expression in organs containing only reserve cells in their epithelium at the onset of the culture. However, corticosterone plus testosterone had a synergistic effect. These data suggest that testosterone promotes the differentiation of principal cells from reserve cells during the culture time and that a primary action of testosterone is necessary to confer corticosterone responsiveness on this tissue. Furthermore, the primary effects of testosterone could be memorized by the tissue because the corticosterone responsiveness persists after castration.     

Effects of estradiol and testosterone on the activity of pyruvate kinase of the cardiac and skeletal muscles of rats as a function of age and sex

The specific activities of pyruvate kinase of cardiac and skeletal (gastrocnemius) muscles of adult rats of both sexes are lower than those of immature rats. The activity does not change after adulthood in the cardiac muscle, but decreases in the gastrocnemius. The activity of pyruvate kinase of the heart of immature and adult rats of both sexes decreases after castration, but is unaffected in old rats. Castration has no effect on the activity of pyrovate kinase of the gastrocnemius muscle of rats of both sexes at any age. In invo administration of estradiol (50 μg/100 g body weight) increases the activity of pyruvate kinase of the heart of castrated male and female rats of the three ages. For the skeletal muscle, the activity increases in castrated adult female and old male rats only. A higher dose (100 μg) of estradiol has variable effects on pyruvate kinase of the heart of male and female castrated rats of different ages. This dose increase pyruvate kinase significantly in the skeletal muscle of old castrated male and female rats. However, it decreases it in the skeletal muscle of adult castrated male rats. Testosterone (100 μm) increases the activity of pyruvate kinase of the heart of castrated male rats. This increase is lower in old age. It has no effect in the heart of castrated female rats of any age. Testosterone (50 μg) increases pyruvate kinase activity of the skeletal muscle of young ovariectomized rats only. A higher dose (100 μg) causes a significant increase in pyruvate kinase of the skeletal muscle of castrated adult and old male, and young and adult female rats, respectively. These data show that sex steroid hormones induce pyruvate kinase of striated muscles, and that the age- and sex-dependent variations may be due to changes in the levels of receptor proteins.     

Localization of beta-endorphin in the rat heart and modulation by testosterone

Chromatographic analysis and radioimmunoassay were used to identify and quantitate beta-endorphin (BE) and beta-lipotropin (B-LPH) in the hearts (devoid of major blood vessels and atria) from intact male rats, castrated male rats, and castrated male rats treated with testosterone propionate (TP). BE and B-LPH in the plasma of these animals were also identified and measured. In comparison to intact animals, castration resulted in a significant elevation in the content of BE in the heart which was reversed by the administration of TP. The content of B-LPH in the heart was not affected by castration or castration in combination with TP. The ratio of BE to B-LPH in the heart of castrated animals was significantly elevated as compared with intact controls. Treatment of castrates with TP returned the ratio of BE to B-LPH to that observed in intact animals. The concentration of BE in the plasma was greater in castrated rats and castrated rats given TP than in intact males, whereas the concentration of B-LPH was diminished in castrated animals given TP. The ratio of BE to B-LPH was greater in castrated animals treated with TP than in castrated and intact animals. The content of BE and B-LPH, as well as the ratios of the two peptides, varied independently in the cardiac tissue and plasma. The present findings indicated that (i) BE and B-LPH are present in cardiac tissue, (ii) the amount of BE and B-LPH in the heart and the ratio of BE to B-LPH appear to be modulated by TP, and (iii) BE and B-LPH detected in the heart was not simply a reflection of the presence of these peptides in the plasma.     

Downward regulation of plasma LH by LHRH agonist, leuprolide acetate, resulting in inhibited renal growth and function in the castrated male rat.

We previously reported that ovine and porcine luteinizing hormone (LH) stimulated kidney growth in castrated hypophysectomized rats. Our present study focuses on the physiological role of the renotropic activity of LH isoforms. Plasma LH levels were decreased to 10% of that of castrated control rats by injections of a slow-releasing LHRH agonist, leuprolide acetate, from microcapsules. Compared to controls, which were injected with microcapsules only, the kidney weight in leuprolide-treated castrated rats decreased 12%. Renal protein and DNA contents decreased significantly. Body, liver and spleen weights were not changed by the treatment, however. This effect on the kidney was not observed in castrated hypophysectomized rats, suggesting that leuprolide affected the kidneys indirectly, rather than directly, by suppressing LH secretion. In leuprolide-treated castrated rats, urinary fractional excretion of sodium (FENa) increased, indicating suppressed renal function at the proximal tubules. We concluded that the secretion of renotropically active LH isoforms was regulated at least partially by LHRH and played a physiological role in growth and the function of the proximal tubules.     

Aphrodisiac properties of Tribulus Terrestris extract (Protodioscin) in normal and castrated rats

Tribulus terrestris (TT) has long been used in the traditional Chinese and Indian systems of medicine for the treatment of various ailments and is popularly claimed to improve sexual functions in man. Sexual behaviour and intracavernous pressure (ICP) were studied in both normal and castrated rats to further understand the role of TT containing protodioscin (PTN) as an aphrodisiac. Adult Sprague-Dawley rats were divided into five groups of 8 each that included distilled water treated (normal and castrated), testosterone treated (normal and castrated, 10 mg/kg body weight, subcutaneously, bi-weekly) and TT treated (castrated, 5 mg/kg body weight, orally once daily). Decreases in body weight, prostate weight and ICP were observed among the castrated groups of rats compared to the intact group. There was an overall reduction in the sexual behaviour parameters in the castrated groups of rats as reflected by decrease in mount and intromission frequencies (MF and IF) and increase in mount, intromission, ejaculation latencies (ML, IL, EL) as well as post-ejaculatory interval (PEI). Compared to the castrated control, treatment of castrated rats (with either testosterone or TT extract) showed increase in prostate weight and ICP that were statistically significant. There was also a mild to moderate improvement of the sexual behaviour parameters as evidenced by increase in MF and IF; decrease in ML, IL and PEI. These results were statistically significant. It is concluded that TT extract appears to possess aphrodisiac activity probably due to androgen increasing property of TT (observed in our earlier study on primates).     

Pulsatile release of immunoreactive luteinizing hormone (irLH) in hypophysectomized male rats

The concentration of plasma luteinizing hormone (LH) was monitored every minute by radioimmunoassay in male rats that were either hypophysectomized, or castrated and hypophysectomized. Castrated rats showed a pulsatile fluctuation of plasma immunoreactive LH (irLH) concentration with an elevated basal level, confirming previous work. The hypophysectomized and castrated hypophysectomized rats also showed pulsatile changes in plasma irLH concentration. This unexpected result indicates that ectopic irLH is not only actively released after hypophysectomy, but is released in pulses. The pulse interval was approximately 20 minutes for all 3 groups. The slope of the rate of decline of plasma irLH in the castrated rats is parallel to a theoretical disappearance rate of 5 min, while these slopes in the hypophysectomized and castrated hypophysectomized rats correspond to a 1 to 2-min disappearance rate. The difference in these slopes implies that the two irLH molecules may not be identical.     

Estrogen influences the effect of immobilization stress on immunoreactive beta-endorphin levels in the female rat pituitary

Immunoreactive beta-endorphin (IR-BE) levels in the plasma, anterior pituitary (AP), the neurointermediate lobe of the pituitary (NIL), and the hypothalamus were determined in castrated female rats and castrated female rats treated with estradiol benzoate (estrogen), after exposure to acute (once for 45 min) or chronic (45 min each day for 15 consecutive days) immobilization stress. Acute and chronic stress increased plasma levels of IR-BE to the same extent in castrated female rats and castrated female rats treated with estrogen. In castrated female rats, acute stress produced an increase in the concentration of IR-BE in the AP, which was attenuated by the administration of estrogen. Although IR-BE in the NIL was not influenced by acute stress in castrated animals, exposure to acute stress resulted in an elevation in IR-BE levels in the NIL of rats given estrogen. Chronic stress did not affect the concentration of IR-BE in the AP of castrated females or castrated females treated with estrogen. Chronic stress did, however, increase the concentration of IR-BE in the NIL of castrated animals. This affect of stress on IR-BE levels in the NIL was potentiated by estrogen administration. IR-BE levels in the hypothalamus were reduced by estrogen and were not affected by acute or chronic stress, regardless of the gonadal steroid environment. As determined by column chromatography, administration of estrogen, as well as subjection to chronic stress, promoted the processing of the proopiomelanocortin precursor to form beta-lipotropin rather than beta-endorphin in the AP. By these methods, the only immunoreactivity detected in the NIL and the hypothalamus was beta-endorphin. These data indicate that IR-BE levels in the plasma, the AP, and the NIL of female rats are affected by immobilization stress and that estrogen modulates the effects of acute immobilization stress on IR-BE levels in the AP and the NIL and the effects of chronic immobilization stress on the levels of IR-BE in the NIL.