Effects Of Pituitary Hormones Research Articles

Panhypopituitarism in adults: modern views and case analysis

The article is devoted to the problem of panhypopituitarism, the diagnosis of which presents certain difficulties in connection with the combined lesion of several peripheral endocrine glands. Modern classification, etiopathogenesis, diagnosis and treatment of the disease are presented. Acquired hypopituitarism in adults develops, as a rule, at the age of 30-60 years, mostly women are affected. Pangypopituitarism is diagnosed when all pituitary tropic functions are affected, which is observed in case of damage to 90% of the adenohypophysis cells. The variety of clinical manifestations of the disease is determined by the different effects of pituitary hormones and the degree of their deficiency. The diagnosis is based on a history of etiological factors causing damage to the pituitary gland, and clinical signs of insufficiency of peripheral endocrine organs, which is confirmed by the results of laboratory studies. In hypopituitarism due to, for example, the growth of pituitary adenoma, the clinical picture develops gradually, and the disorder of the secretion of the pituitary tropic hormones usually occurs in the following sequence: the production of somatotropic hormone, gonadotropins, then thyrotropic hormone, adrenocorticotropic and, lastly, prolactin decreases. Neurosurgery or hemorrhage in the pituitary gland causes a rapid manifestation of the disease, and the severity of the condition is associated mainly with adrenal insufficiency. In the case of surgery for pituitary adenoma, there is a recommendation to determine morning blood cortisol on the 3rd day after surgery. Conservative treatment is aimed at compensating for hormone deficiency. According to the clinical significance of endocrine disorders, their correction is carried out in the following sequence — first, compensation for adrenal insufficiency, then thyroid, sex glands and somatotropin. In case of damage to the posterior lobe of the pituitary gland with the development of diabetes insipidus syndrome, replacement therapy for vasopressin deficiency is also required. The clinical example presented in the article reflects the difficulty of diagnosing and interpreting the data of hormonal studies in panhypopituitarism. An analysis of the described clinical situation shows the importance of understanding the pathogenesis of the disease when conducting a diagnostic search. Adequate replacement therapy can restore normal well-being in patients with hypopituitarism.

Hypophysectomy enhances interleukin-1beta, tumor necrosis factor-alpha, and interleukin-10 mRNA expression in the rat brain.

Although the effects of various cytokines as regulators of hormone synthesis and production are well documented, the role for pituitary hormones as modulators of cytokine synthesis is not fully understood. In this study, we investigated the effect of pituitary hormones' depletion on cytokine synthesis after short- (21 days) and long- (35 days) term hypophysectomy (ST-HX and LT-HX, respectively). The expresssion of the proinflammatory cytokine interleukin-1beta (IL-1beta) and tumor necrosis factor-alpha (TNF-alpha) and the anti-inflammatory cytokines IL-10 and transforming growth factor-beta (TGF-beta) in the rat brain was studied using in situ hybridization. Our results indicate that IL-1beta mRNA-expressing cells were significantly upregulated at day 21 in hypophysectomized rats compared to sham-operated controls. This enhanced expression was also detected later at day 35 post hypophysectomy. However, TNF-alpha mRNA expression was significantly increased only at the later sampling interval. IL-10 mRNA-expressing cells were increased after long-term hypophysectomy compared to controls. TGF-beta mRNA-expressing cells were not increased after hypophysectomy. In conclusion, these results suggest a role for pituitary hormones in IL-1beta, TNF-alpha, and IL-10 synthesis.

Effects of pituitary hormones on the prostate.

Although essential, androgens alone are not sufficient to induce normal growth and functionality of the prostate. Nonandrogenic hormones must also be involved in the proliferation of the prostate cancer cells which do not respond to antiandrogenic therapy and which thus become androgen-independent. Prolactin, but also growth hormone and luteinizing hormone, are potentially able to act on both normal and abnormal prostatic cells. In this review we summarize data from the literature concerning the physiological and pathological implications of prolactin, growth hormone, and luteinizing hormone on the prostate. In rodent prostates, prolactin and growth hormone can induce a variety of effects independently of androgens (e.g., transactivation of certain genes, or synthesis of the major secretion products). Moreover, hyperprolactinemia is responsible for inflammation and dysplasia of the gland, while growth hormone promotes the development of prostate tumors in vivo in the mouse and rat. Growth hormone acts on the gland directly, through prostatic growth hormone receptors, and/or indirectly via the stimulation of insulin-like growth factor-I (IGF-I) synthesis in the liver. Luteinizing hormone receptor is expressed in rat and human prostates. Luteinizing hormone increases the amount of various transcripts in the rat prostate through an androgen-independent pathway. Prolactin, growth hormone, and luteinizing hormone, alone or synergistically with androgens, play physiologically significant roles in the normal prostate. The involvement of these hormones in the development of benign prostatic hyperplasia and prostatic carcinoma is an issue that needs to be addressed.

Pituitary control of proliferation and differentiation of Leydig cells and their putative precursors in immature hypophysectomized rat testis.

The objective of this study was to determine the effects of pituitary hormones (luteinizing hormone [LH], follicle-stimulating hormone [FSH], growth hormone [GH], and prolactin [PRL]) on interstitial cell proliferation and differentiation in the testis of immature hypophysectomized rats. Macrophages, Leydig cells, precursor mesenchymal cells, endothelial lymphatic cells, and myoid cells were studied. Our experimental approach was aimed at determining whether changes in a cellular subpopulation observed after pituitary hormone treatments were the result of division of existing cells in the population, of differentiation of interstitial precursor cells, or both. In this context, it must be stressed that our data reflected the effects of hormones to prevent the decline of cells due to hypophysectomy rather than their recovery. Macrophage proliferation was taken into account because macrophages closely resemble Leydig cells and are known to proliferate after hormonal treatment. A double-labeling procedure (acid phosphatase and anti-bromodeoxyuridine [anti-BUdR]) revealed that LH, FSH, and PRL increased the number of testicular macrophages 105-, 104-, and 103-fold, respectively, in hypophysectomized rats compared to hypophysectomized control animals. BUdR incorporation in testicular macrophages was greater after PRL treatment than after LH and FSH supplementation. In contrast, we were unable to demonstrate any effect of rat GH on the macrophage population. Light microscopic analysis of plastic embedded sections of treated rat testis revealed that LH increased the numbers of Leydig, precursor mesenchymal, and myoid cells 6-, 4-, and 1.3-fold, respectively. LH also stimulated BUdR incorporation into all interstitial cell types. PRL administration increased both the number of Leydig and precursor mesenchymal cells (each 3-fold) but decreased the number of endothelial lymphatic cells (1.5-fold) when compared to the control animals. In contrast, FSH did not increase the number and proliferation of Leydig cells but exerted a slight proliferative effect on the other interstitial cell populations. In GH-treated rats, the number of precursor mesenchymal cells increased two fold above the control rats. GH also exerted slight proliferative effects on both precursor mesenchymal and myoid cells. Immunohistochemical studies of steroidogenic enzymes in the testicular interstitium of treated rats demonstrated the presence of steroidogenic enzymes, not only in Leydig and precursor mesenchymal cells, but also in some (1%-2%) endothelial lymphatic cells and myoid cells. This may indicate that both of these cell types are also constitutively equipped to perform steroidogenesis or that they are precursor cells undergoing differentiation. Taken together, changes in the number of Leydig cells in our animal model appeared more likely to be dependent on the transformation of precursor cells than on division of preexisting mature Leydig cells.

Pituitary hormones as neurotrophic signals: anomalous hypophysiotrophic neuron differentiation in hypopituitary dwarf mice.

Anterior pituitary hormones are known to exert dynamic negative feedback effects on their respective regulatory ("hypophysiotropic") neurons in the hypothalamus. The purpose of this review is to present the evidence for a theory that the effect of pituitary hormones on these hypophysiotropic neurons is neurotrophic, extending beyond dynamic feedback to influence upon cell survival, phenotypic differentiation, and axonal connectivity. To that end, the adult condition and the development of hypophysiotropic neurons in mutant mice which lack pituitary growth hormone (GH) and prolactin (PRL) are presented as models of the effect of absent specific neurotrophic signals. The expression of the neurohormones which inhibit PRL and GH secretion, dopamine (DA) and somatostatin, respectively, is markedly reduced in the hypothalamus of the hypopituitary dwarf mouse, and this adult condition is the result of postnatal failure to develop or actual regression, which may include neuronal cell death. The deficit in DA may be reversed by PRL replacement, but only if initiated at an identified critical postnatal period. Conversely, expression of the stimulatory GH-releasing hormone (GHRH) is markedly increased in the dwarf mouse hypothalamus. The loss of DA and the increase in GHRH occur in the same hypothalamic area, suggesting neuronal phenotypic plasticity in response to absence of pituitary feedback signals. The axonal terminations of extant GH- and PRL-regulating neurons in external median eminence appear to be reduced, suggesting that pituitary signals are required for appropriate axonal guidance during development, even though an endocrine vascular route intervenes between these regulatory neurons and their target secretory cells. The collective observations indicate that GH and PRL may be regarded as neurotrophic factors for their respective regulatory neurons in the hypothalamus.

Effects of pituitary hormones on the cell-specific expression of the KAP gene

The expression of kidney androgen-regulated protein (KAP) gene in mouse kidney is regulated in a multihormonal fashion. As determined by in situ hybridization analysis, epithelial cells of proximal convoluted tubules of cortical nephrons express KAP mRNA in response to androgenic stimulation while similar cells in the juxtamedullary S3 segment of the tubules express KAP mRNA under estrogenic and pituitary hormonal control. In situ hybridization analysis of kidney sections using hypophysectomized (hypox) mice resulted in a total absence of KAP mRNA suggesting the participation of a pituitary hormone(s) in the constitutive expression of KAP mRNA in S3 cells. Treatment of hypox mice with steroid hormones showed that androgens restored the ability of cortical tubule cells to synthesize KAP mRNA. Estrogen treatment, on the other hand, partially induced KAP gene expression only in S3 cells. These results indicated that the androgenic response of the gene is independent of pituitary function, while expression in S3 cells, although partially induced by the direct action of estrogens, is primarily regulated by a pituitary factor. In order to elucidate which hormone(s) is responsible for KAP gene expression in S3 cells, individual pituitary hormones were administered to hypox normal animals and to strains of mice genetically deficient in certain pituitary hormones. Surgically treated C57BL/6 female and male mice were implanted for 7 days with osmotic pumps containing individual pituitary hormones, after which the kidneys were analyzed by in situ hybridization. Mice injected with growth hormone (GH), corticotropin (ACTH), prolactin (PRL), or vehicle failed to express KAP mRNA. Mice treated with thyrotropin (TSH), follitropin (FSH), and lutropin (LH) exhibited high levels of KAP mRNA in S3 cells of females as well as in the renal cortex of male animals. Expression in the cortex in response to LH and FSH may be due to their gonadotropic effect on testosterone production. Similarly, contamination of TSH samples with small amounts of the gonadotropins may explain the cortical response to TSH. TSH produced the strongest response in S3 cells suggesting that it is responsible for the permissive effect of the pituitary on KAP gene expression. This conclusion was supported by studies performed with the dwarf mouse ( dw/dw) which lacks PRL, GH, and TSH due to a mutation in the pit-1 gene. In situ hybridization analysis of dwarf mice kidney sections showed a complete lack of KAP gene expression. The possible participation of GH and PRL was eliminated on the basis of the hormone replacement studies. In addition, involvement of GH was excluded by the observation that GH-deficient little mice express KAP mRNA in S3 cells. Taken together, these data indicate that TSH is necessary for KAP gene expression in the epithelial cells of the S3 segment of the proximal tubules.

Roles of pituitary hormones in the regulation of hepatic cytochrome P450IIE1 in rats and mice

Cytochrome P450IIE1 (P450IIE1) is responsible for the metabolic activation of N-nitrosodimethylamine (NDMA), a potent environmental carcinogen. This P450 enzyme displays a high-affinity NDMA demethylase (NDMAd) activity and is known to be induced by fasting and acetone administration. In the present work, the effects of pituitary hormones on the regulation of P450IIE1 in the liver were investigated and compared in rats and mice. There was no difference in liver microsomal NDMAd activity (nmol/min/mg protein) in rats in the intact (0.38 ± 0.12), sham-operated (0.44 ± 0.06), and hypophysectomized (0.52 ± 0.04) groups. However, hypophysectomy caused a 2-fold increase in hepatic P450IIE1 protein levels as determined by immunoblot analysis. The P450IIE1 mRNA level in hypophysectomized rat was also significantly increased. The levels of blood ketone bodies (acetone, acetoacetate, and β-hydroxybutyrate) were not different in the intact, sham-operated, and hypophysectomized groups, suggesting that ketone bodies are not involved in the induction of P450IIE1 protein and its mRNA by hypophysectomy. The discrepancy between the NDMAd activity and the increased P450IIE1 protein in rat liver by hypophysectomy can be partially explained by the lower hepatic NADPH-P450 reductase activity (50% that of the control) in the hypophysectomized rats. Upon the induction of liver NDMAd activity by fasting and acetone, hypophysectomy attenuated the effect of acetone but abolished the effect of fasting completely. Nevertheless, fasting still caused a 3-fold increase in the liver P450IIE1 mRNA level. An involvement of pituitary hormones in the regulation of liver microsomal P450IIE1 in mouse, however, was not observed. There was no difference in constitutive NDMAd activity between genetically growth hormone-deficient ( lit/lit) mice and their phenotypically normal heterozygotes ( lit/+). Fasting for 48 h caused 1.5- to 2-fold induction and acetone caused 2- to 3-fold induction, in both groups. The above changes in enzyme activity were due to the changes of P450IIE1 levels as verified by the immunoblot analysis. In male BALB/c mice, neither the hepatic NDMAd activity nor the P450IIE1 protein level was altered by hypophysectomy. The effects of acetone on the liver NDMAd activity were also similar in hypophysectomized and sham-operated mice. The results suggest that pituitary hormones are important in the regulation of the expression and activity of hepatic P450IIE1 in rats but not in the mouse strains investigated.

Endocrine Factors Affecting Thyroid Economy of Teleost Fish

SYNOPSIS. This review examines the way in which the activity of the hypothalamo-pituitary-thyroid axis in teleost fishes is modified by pituitary, steroid and amine hormones. These factors may act at the level of the hypothalamus, the pituitary gland (thyrotrops), the thyroid gland, or the peripheral tissues, and affect thyroid hormone synthesis, release, metabolism, or degradation. With few exceptions, the studies are limited to only a few species, the results are often fragmentary and contradictory, are based on experiments in which pharmacological, rather than physiological, hormone ranges have been used, and there is too little information to establish a consistent pattern of response to endocrines other than those which are components of the hypothalamo-pituitary-thyroid axis itself. Most studies evaluating the effects of pituitary hormones on thyroid economy in fish have, of necessity, relied on mammalian preparations. Some of these ( e.g. , prolactin and the gonadotropins) elicit very different responses from those of the equivalent semipurified or purified piscine hormone, although mammalian and piscine TSH and GH respectively appear to elicit similar responses in the teleostean thyroid system. The elevation of plasma T4 levels in response to a challenge of exogenous TSH has been used in several studies as a way of evaluating the sensitivity of the thyroid to TSH; the response is modified by photoperiod, season, stage of development, estrogen and corticosteroids.

O-57) - Effect of pituitary hormones on carboxylesterase and drug metabolizing enzymes in rat liver microsomes

O-57) - Effect of pituitary hormones on carboxylesterase and drug metabolizing enzymes in rat liver microsomes

The effects of pituitary hormones on hepatic drug metabolism in the rat

Sex differences exist in the hepatic microsomal metabolism of drugs in the rat. These differences have been shown to be related to the presence of androgen in the male and the pituitary gland in the female. The present study was designed to identify the pituitary 'feminizing factor' by continuously infusing hormones via an osmotic mini-pump. Rat somatotropin and prolactin mimicked somewhat the 'feminizing' effect of pituitary extract infused into male animals while human somatotropin, which binds to both lactogenic and somatogenic receptors in rat liver, completely reversed the effect of hypophysectomy of female rats with respect to most of the parameters studied. It thus appears that the somatogenic/lactogenic receptors in the rat liver are involved in the maintenance of the sex differences in drug metabolism but the identity of the hormone that normally acts on these receptors in the rat is still uncertain.

Induction of testicular gonadotropin-releasing hormone (GnRH) receptors by GnRH: effects of pituitary hormones and relationship to inhibition of testosterone production.

In vivo administration of gonadotropin-releasinghormone (GnRH) inhibits testosterone production in intact rats and increases testicular GnRH receptors. To delineate the relationship of these effects and to determine whether GnRH induced its testicular receptor by an extrapituitary mechanism, GnRH and LH receptors were studied in intact or hypophysectomized (H) rats. Adult, H, or sham-operated (S) males were injected with GnRH (6.7 μg every 8 h for 1, 2, 4, and 6 days). Some H rats were also treated with GH and PRL (150 μg/day) to maintain LH receptors. Decapsulated testes were assayed for GnRH and LH receptors or incubated to assess testosterone production in the presence or absence of hCG. GnRH treatment in S rats resulted in a biphasic change in GnRH receptor numbers. The basal receptor concentration (212 ± 27 fmol /mg protein) increased to a peak at 2 days (501 ± 32 fmol/mg) before declining to control values after 6 days of treatment. GnRH receptors increased 2-fold 1 day after hypophysectomy (449 ± 5...

Effect of pituitary hormones on phosphodiesterase and adenylate cyclase activity in brain tissuein vitro

Effects of seiwhale somatotropin (STH), its biologically active fragment 77--107, porcine corticotropin (ACTH) and seiwhale prolactin on phosphodiesterase and adenylate cyclase activity of glial cells and synaptosomes isolated from the rat brain cortex were investigated. As compared with control, ACTH increased phosphodiesterase activity of glial cells by 392%, of synaptosomes by 123%, while STH by 49 and 77%, respectively, somatotropin fragment by 455 and 74%, and prolactin by 30 and 37%, respectively. Adenylate cyclase activity was significantly changed only by ACTH and only in synaptosomes (a 50% decrease). STH, its fragment and prolactin virtually failed to alter adenylate cyclase activity. The data obtained indicate that some of pituitary hormones, primarily ACTH and STH, may play the role of neuromodulators in some brain structures by decreasing the cyclic AMP level, by activating phosphodiesterase (STH and ACTH) and inhibiting adenylate cyclase (ACTH in synaptosomes).

Effect of pituitary hormones on alpha-amino-beta-carboxymuconate-epsilon-semialdehyde decarboxylase in rat.

The hormonal regulation of α-amino β-carboxymuconate-e-semialdehyde decarboxylase (picolinic carboxylase) was studied to clarify the change of tryptophan-niacin metabolism in the different physiological states. Hypophysectomized rats were administered with predonine hemisuccinate and various kinds of pituitary hormones for 2 or 4 days every 12 hr. The activity of their liver picolinic carboxylase was then assayed. The injection of predonine alone elevated the enzyme activity in hypophysectomized rats. On the other hand, rat or bovine pituitary extract was found to suppress such enzyme induction when it was administered prior to predonine injection. The enzyme-suppressing activity of the pituitary extract was lost by heat treatment or addition of proteolytic enzyme such as trypsin and chymotrypsin. These results indicate that the effective substances in the extract may be polypeptides. By gel filtration of bovine pituitary extract, two effective fractions were obtained, which were able to suppress the predonine-dependent induction of liver picolinic carboxylase. The molecular weights of these substances were estimated to be about 23, 000 and 2, 000-4, 000, respectively. Both of these effective substances were shown to be localized in the anterior lobe of hypophysis. In the many kinds of pituitary hormones tested, bovine somatotropin and mammalian prolactin were found to be effective in suppressing the predonine-dependent induction of liver picolinic carbo xylase in hypophysectomized rats. To obtain some information on the mechanism by which liver picolinic carboxylase activity is elevated in diabetic rats, bovine somatotropin or rat pituitary extract was administered to diabetic rats for 4 or 7 days every 12 hr. This hormone treatment was not observed to depress the enzyme activity in the diabetic rats. These results are considred to suggest that changes in pituitary hormone are not responsible for the elevation of the enzyme activity in the diabetic rat.

Effect of pituitary hormones on dentin production in maxillary incisors in the rat

The effect of pituitary hormones on dentin production and longitudinal growth of the maxillary incisors in normal and hypophysectomized rats was investigated. Bovine growth hormone was found to increase the dentin production slightly in normal rats and significantly in hypophysectomized rats. Other pituitary hormones showed no effects on dentin apposition in the doses and periods tested. The effects of the pituitary hormones on the longitudinal growth of the tooth were small or insignificant. The effects of growth hormone on the dentin apposition and the longitudinal growth of the tooth after hypophysectomy were smaller than the effects on longitudinal bone growth and cortical bone remodeling, indicating different sensitivity to hormones between different mineralized tissues.

Learning and Behavior (I): Effects of Pituitary Hormones

Learning and Behavior (I): Effects of Pituitary Hormones

Effects of hypophysectomy, bilateral adrenalectomy and hormone replacement therapy upon organ monoamine oxidase activity

Changes in MAO activity after hypophysectomy (HX) are not due to adrenal insufficiency. ACTH failed to reverse the effects of HX and enhanced the depression of cardiac and spleenic MAO. The data suggests both facilitatory and inhibitory effects of pituitary hormones on MAO activity.

Effects of pituitary hormones and corticosterone on lipolysis in hypophysectomized rats.

ABSTRACT Removal of the pituitary gland in rats reduces basal lipolysis and greatly diminishes the lipolytic response of isolated fat cells towards L-epinephrine, ACTH and dibutyryl-cyclic-3′5′-AMP (DB-cAMP). Subcutaneous application for 5 days of ACTH, LH, FSH, GH and TSH, single or in combination, does not appreciably influence the responsiveness of fat cells towards lipolytic stimulation. Administration of a hypophyscal homogenate restores the sensitivity of fat cells of hypophysectomized rats. A similar effect is obtained with a combination of growth hormone and corticosterone. In hypophysectomized-adrenalectomized animals only the combination of growth hormone and corticosterone, but not a pituitary homogenate, produces a normal responsiveness of fat cells towards lipolytic stimuli. It is concluded that both the pituitary and adrenal gland are intimately involved in the hormonal regulation of lipolysis in fat cells.

Effect of neonatal administration of prolactin on pituitary secretion of prolactin and gonadotrophins in adult female rats.

In female rats neonatal treatment with oestrogen induces persistent vaginal cornification and sterility at maturity (Takewaki, 1962). Recently, we found that the pituitary secretion of prolactin, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in such oestrogenized female rats is permanently altered (Nagasawa, Yanai, Kikuyama & Mori, 1973). No data are available, however, on the effect of pituitary hormones, administered neonatally, on the secretory activity of the pituitary in adult rats. In the present experiment the pituitary secretion of prolactin, LH and FSH was measured in adult female rats treated neonatally with prolactin. Virgin female Sprague—Dawley rats were used. Half the females in each litter were given a daily subcutaneous injection of bovine prolactin (NIH-P-B2) dissolved in 0·25–1·0 ml 0·9% NaCl solution (pH 8) for 20 days beginning on day 0 of age. The dose of prolactin was 0·5 mg for the first 5 days, 1·0 mg for the second 5

Effects of pituitary hormones, melatonin, and thyroidal inhibitors on radioiodide uptake by the thyroid glands of larval and adult tiger salamanders, Ambystoma tigrinum (Amphibia: Caudata)

Thyroidal uptake of radioiodide 24 hr after intraperitoneal injection of 131I was used as a measure of thyroidal function in the tiger salamander ( Ambystoma tigrinum). Larvae pretreated for 7 days with 2.5 or 25 μg TSH/day exhibited significantly greater 131I uptake than did untreated animals. Spontaneously metamorphosing animals accumulated 131I equivalent to larvae pretreated with 2.5 μg TSH. Fully metamorphosed animals were insensitive to pretreatment with 2.5 μg TSH/day, but did respond to 25 μg TSH/day. PTU or SCN pretreatment of larvae reduced TSH-stimulated 131I uptake to control levels, but prolactin, melatonin, and bovine pineal extract had no effect. Prolactin treatment of larvae (7 or 60 days) did not influence 131I uptake as compared to controls. Thyroidal 131I uptake in metamorphosed animals was not influenced by 7 days of treatment with prolactin. Daily pretreatment (7 days) with 25 μg LH or FSH or 0.25 μg TSH did not increase 131I accumulation by larvae. Mammalian prolactin and gonadotropins apparently are not heterothyrotropic factors in this species. The stimulation of metamorphosis by mammalian gonadotropins (Norris et al., 1973b) can be attributed to the amount of mammalian TSH present in these preparations.

Effect of pituitary hormones, androgens, and corticosteroids on the seminal vesicles of the castrate catfish, Heteropneustes fossilis (Bloch).

AbstractΔ5‐3β‐hydroxysteroid dehydrogenase activity (Δ5‐3β‐HSD) has been studied in the interrenal glands and the seminal vesicles of intact and castrate male catfish. The intensity of the enzyme reaction is about equal in the seminal vesicles of both groups, whereas the intensity of enzyme reaction in the cortical cells is more pronounced in the castrate than in the intact male.The responses of the interrenal glands and the regressed seminal vesicles of the castrate catfish in the postspawning period to exogenous luteinizing hormone (LH), Δ4‐androstenedione (Δ4‐androst.), desoxycorticosterone acetate (DCA) and hydrocortisone acetate (HA) (experiment 2), and the effect of the LH, Δ4‐androst., DCA and HA, and prolactin (LtH) and growth hormone (STH), singly or in combination on the regressed seminal vesicles of the castrate catfish (experiment 3) have also been studied. The data indicate that both LH and Δ4‐androst. induce secretory activity in the seminal vesicles but they appear to act through different routes. Since LH brings about an increase in the nuclear diameters in cortical cells and Δ4‐androst. does not, it is felt that LH acts through the cortical cells of the interrenal glands while Δ4‐androst. acts directly on the seminal vesicles. Further, Δ4‐androst. can synergize with LtH and STH in inducing secretory activity in the seminal vesicles, whereas DCA and HA do not. These results, coupled with the fact that Δ5‐3β‐HSD activity is more marked in the cortical cells of the castrate than in the intact catfish, strongly suggest that following castration, the resulting high titers of gonadotrophin act on the interrenal cortical cells to produce androgens which, in turn, induce hyperactivity in the seminal vesicles.