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PubMed2002

Four cardiac hormones increase circulating concentrations of luteinizing hormone and testosterone.

This study was designed to determine whether four peptide hormones consisting of amino acids 1-30-long-acting natriuretic hormone (LANH), 31-67 (vessel dilator), 79-98 (kaliuretic hormone), and 99-126 (atrial natriuretic hormone [ANH])-of the 126 amino acid atrial natriuretic prohormone increase the circulating concentration of testosterone in healthy humans (n = 30). Vessel dilator, kaliuretic hormone, LANH, and ANH increased the circulating concentration of testosterone 3.8, 2.6, 3.9, and 3.4-fold, respectively (p < 0.01 for each), when infused at 100 ng/(kg of body wt . min) for 60 min. The increases in testosterone lasted 2.5-3 h after cessation of the respective atrial natriuretic peptides' infusions. ANH, vessel dilator, LANH, and kaliuretic hormone increased luteinizing hormone (LH) 3-to 8.4-fold (p < 0.001) during infusion, with the maximal increase in LH being 6.7- to 11.7-fold (p < 0.001) secondary to these cardiac hormones. Vessel dilator and kaliuretic hormone increased LH before increasing testosterone in a sequential fashion. These data suggest that four peptide hormones-ANH, LANH, vessel dilator, and kaliuretic hormone-increase the circulating con-centrations of LH and testosterone in humans.

Adult↗
PubMed1975

Immunological identity of human and porcine growth hormones. Application to determination of growth hormone in porcine serum.

In two radioimmunoassay systems with iodinated human growth hormone as tracer and anti-human growth hormone or anti-porcine growth hormone as binding site, the standard curves for human and for porcine growth hormone were parallel. In both systems the porcine growth hormone preparation had to be added in about the same excess as compared to the human hormone. It was concluded that the human and the porcine hormones behave in an identical way and that the values obtained in radioimmunoassay for human growth hormone represent the amount of immunologically active molecules in the porcine growth hormone preparation. As parallel standard curves were obtained with porcine serum, the concentration of growth hormone is porcine serum may be determined by radioimmunoassay for human growth hormone.

Animals↗
PubMed2003

An expression study of hormone receptors in spontaneously developed, carcinogen-induced and hormone-induced mammary tumors in female Noble rats.

The Noble (Nb) rat model has been used in the study of hormonal carcinogenesis of mammary and prostate glands, as this rat strain is susceptible to tumor induction in these glands by hormonal treatments. Recently, we demonstrated that this rat strain can develop spontaneously mammary tumors at high incidence in aged animals and also show high sensitivity to chemical carcinogens (DMBA and MNU) and combined treatments with sex hormones in mammary tumor induction. In the present study, we examined and compared the expression of hormone receptors [including estrogen receptors (ERalpha and ERbeta), androgen receptor (AR), progesterone receptor (PR), prolactin receptor (PRLR)] and prolactin (PRL) by immunohistochemistry, Western blotting and RT-PCR in spontaneous mammary tumors, and mammary tumors induced by sex hormones (T+E2 and T+DES for 8-10 months) and DMBA in Nb rat model. Immunohistochemistry and Western blotting showed that both the spontaneously developed and hormone-induced carcinomas exhibited strong immunoreactivity of ERalpha, ERbeta, AR, PR and PRLR, while the spontaneous fibroadenomas showed weak to moderate immunoreactivity of ERalpha and PRLR, whereas the DMBA-induced carcinomas exhibited weak to moderate immunoreactivity of ERalpha, AR, PR and PRLR, and sporadic weak ERbeta immunoreactivity. RT-PCR analyses showed that mRNA expression pattern of these markers resembled that of proteins. In addition, weak mRNA expression of PRL was detected in spontaneous carcinomas and carcinomas induced by DMBA and hormones, suggesting that PRL could be produced locally within the tumors. The results showed that the expression status of hormone receptors and PRL was different in spontaneous mammary tumors and tumors induced by carcinogen or hormones, suggesting that the extent of involvement of steroid hormones and their receptors in the spontaneous, carcinogen- or hormone-induced mammary carcinogenesis might be different.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1986

Alterations in local chromatin structure accompany thyroid hormone induction of growth hormone gene transcription.

The chromatin structure of the growth hormone gene and flanking DNA was analyzed in GC rat pituitary tumor cells, which appropriately express and regulate the gene. Thyroid hormone induced the DNase I hypersensitivity of a chromatin domain spanning the transcriptional initiation site from approximately -200 to +150. Three inducible hypersensitive sites were discerned in this region. One of these sites was in the first intron of the gene. The second site was within a region of 5' flanking DNA which promotes accurate, thyroid hormone-regulated transcriptional initiation. Centered between these two sites was a third hormone-inducible hypersensitive site mapping at the position of the TATA sequence. The hormone responsiveness of these hypersensitive sites suggests that occupied 3,5,3'-triiodo-L-thyronine receptor interacts with sequences flanking the growth hormone promoter, perhaps facilitating the binding or activation of a transcription factor at the TATA homology. Three hormone-independent hypersensitive sites were identified near or within intron or flanking DNA sequences similar to Chinese hamster ovary type 2 repetitive DNA. Two additional hormone-independent hypersensitive sites were located more than 1000 nucleotides up-stream of the growth hormone promoter. These sites were present in the cloned genomic DNA and were the only distinct sites found in rat spleen and cultured rat liver cells. Thyroid hormone treatment of GC cells appeared to increase the moderate DNase I sensitivity of the growth hormone gene region beyond that found in deinduced or glucocorticoid-treated cells. Dexamethasone had no discernible effect on the chromatin structure of the gene or flanking DNA in these studies.

Animals↗
PubMed1987

Discrete positive and negative thyroid hormone-responsive transcription regulatory elements of the rat growth hormone gene.

We have recently shown that a thyroid hormone-responsive transcription stimulatory element exists in the 5'-flanking DNA near the rat growth hormone (rGH) gene (Crew, M. D., and Spindler, S. R. (1986) J. Biol. Chem. 261, 5018-5022). Progressive deletion-transfection analysis of the 5' end of the gene has led to the identification of two genetic elements responsive to thyroid hormone. The first of these is a thyroid hormone-responsive transcription stimulatory element, or TSE. The TSE induced a thyroid hormone-dependent induction-attenuation transcription cycle similar to that of the natural rGH gene. Deletion of sequences between positions -254 and -241 in the rGH 5'-flanking DNA eliminated TSE activity. The second regulatory element is a thyroid hormone-responsive transcription inhibitory element (TIE). When this element was active, thyroid hormone strongly but transiently inhibited rGH promoter utilization. Deletion of sequences between nucleotides -46 and -21 abolished the effects of the TIE. To determine whether the TSE and TIE are enhancer-like, we ligated various regions of rat growth hormone 5'-flanking DNA containing these elements to a chimeric test gene containing the Herpes simplex virus thymidine kinase promoter. Thyroid hormone activated heterologous promoter utilization when a rat growth hormone 5'-flanking DNA fragment containing the TSE (-520 to -115) was linked in cis, regardless of the distance or orientation of the TSE with respect to the promoter. These data suggest that the TSE is a thyroid hormone-dependent enhancer. In contrast, when the TIE was placed immediately 5' to the thymidine kinase promoter, transcription was not effected by 3,5,3'-L-triiodothyronine, suggesting that the TIE is not enhancer-like.

Animals↗
PubMed1994

Plasma concentrations of FSH, LH, thyroid-stimulating hormone and growth hormone after exogenous stimulation with GnRH, TRH and GHRH in Booroola ewes that are homozygous carriers or non-carriers of the FecB gene.

The aim of the present study in Booroola ewes, either homozygous (BB) or non-carriers (++) of the FecB gene, was to test the specificity of the pituitary responses to exogenous hypothalamic releasing hormones by examining the plasma concentrations of FSH, LH, thyroid-stimulating hormone (TSH) and growth hormone (GH) after injecting the animals with different doses of GnRH, thyroid-releasing hormone (TRH) or growth-hormone-releasing hormone, (GHRH) which were administered on separate occasions. The animals (n = 8 per dose) received 0, 3.1 or 12.5 micrograms of thyroid-releasing hormone and GnRH (i.v.), whereas they (n = 9-13 per dose) received 0, 6.0 or 16.0 micrograms GHRH (i.v.). For each experiment there were no differences between the genotypes in bodymass or age. Gene-specific differences in the mean pretreatment concentrations of plasma FSH (BB > ++; P < 0.05) but not of LH, TSH or GH were noted. After treatment with GnRH, TRH or GHRH, significant effects of dose were noted for all the hormones; however, a gene-specific effect was observed only for FSH in response to GnRH (BB > ++; P < 0.01) with no genotype x dose interaction (ANOVA). For LH, the effects of genotype and the genotype x dose interaction almost reached significance at the 5% level (genotype, P = 0.055; genotype x dose, P = 0.067). For TSH and GH the respective genotype x dose interactions were not significant.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

[Hypothalamic pituitary function in brain death patients--from blood pituitary hormones and hypothalamic hormones].

According to the report of the Health and Welfare Ministry's research committee on brain death (1985), "brain death is defined as an irreversible cessation of the total brain function including brain stem." However, in brain death patients, whether the hypothalamic function which belongs to the brain stem function has completely ceased or not is unknown. In order to evaluate the hypothalamic function in brain death patients, the blood levels of the pituitary hormones and hypothalamic hormones were measured, and anterior pituitary stimulation test with triple bolus injection (TRH 500 micrograms, LH-RH 100 micrograms, regular insulin 0.3-0.7 unit/kg) was performed. The subjects were 13 brain death patients whose clinical states fully satisfied the criteria proposed by the committee. 1) The average blood levels of anterior pituitary hormones in these brain death patients were within normal range, and that of growth hormone was more than the twice of the normal level. 2) The blood anterior pituitary hormones were detectable in almost all cases even several days after the diagnosis of the brain death. 3) LH reserve was maintained in three cases. FSH reserve was maintained in three cases. Prolactin reserve was maintained in two cases. TSH reserve was maintained in one case. 4) Blood ADH (antidiuretic hormones) were detectable in 7 cases out of 9 cases. The blood ADH level of one case, in particular, was rather high (above 10 pg/ml). 5) Histopathologically anterior pituitaries were examined in three autopsy cases. The central necrotic areas were observed in all cases, but normal pituitary tissues existed peripherally. And all anterior pituitary hormones could be recognized immunohistochemically. 6) The blood levels of the hypothalamic hormones (GRF, CRF, LH-RH) were measured in four cases. The hypothalamic hormones were detectable in all cases. In one case, the levels of GRF were within normal range even 9 or 15 days after the diagnosis of brain death.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2000

Changes in concentrations of plasma immunoreactive follicle-stimulating hormone, luteinizing hormone, estradiol-17beta, testosterone, progesterone, and inhibin in heifers from birth to puberty.

This study was designed to clarify the characteristics of changes in plasma concentrations of reproductive hormones in heifers from birth to puberty. Weekly or daily hormonal changes were observed in 39 heifers. Daily changes in the concentration of follicle-stimulating hormone (FSH) demonstrated a consistent cycle of hormone changes over a 7- to 8-day period in heifers from approximately 10 days to 9 months old. Weekly changes in reproductive hormones showed that there were three brief periods in heifers between birth and puberty in which dramatic changes occur. The first period was the first week after birth, during which a reciprocal relationship between steroid hormones and gonadotropins was observed. At birth, the concentrations of steroid hormones were higher than those at any other age. These hormone levels rapidly decreased within the first week after birth. Gonadotropin levels, however, increased from birth to 1 week of age. The second period of major change was at approximately 4 weeks of age when there was an increase in the concentrations of luteinizing hormone (LH), estradiol-17beta, testosterone, and immunoreactive inhibin. The third period was the last 5 weeks before the first ovulation, when there was an increase in the concentrations of estradiol-17beta followed by an increase in (LH). These results suggest that regular hormone changes start from 10 days after birth and that the periods from birth to 4 weeks of age and the last 5 weeks before the first ovulation in heifers are important to the development of reproductive functions before puberty.

Animals↗
PubMedDate not supplied

Transcriptional regulation of growth hormone gene expression by growth hormone-releasing factor.

Production and release of hormones by the pituitary is known to be under complex hormonal control. Prolactin, for example, is both positively and negatively regulated by steroid and thyroid hormones as well as by peptide hormones. Some hypothalamic releasing factors have been shown to regulate both hormone biosynthesis and hormone release. In the case of growth hormone (GH), glucocorticoids and thyroid hormone stimulate its production, at least in part by stimulating transcription of the GH gene, and somatostatin inhibits and growth hormone-releasing factor (GRF) stimulates its release. So far, however, polypeptide hormone regulation of GH biosynthesis has not been demonstrated. Recently a peptide with GH-releasing activity has been characterized from human pancreatic islet tumours. We report here that pure human pancreatic GRF (hpGRF) stimulates transcription of the GH gene, as well as stimulating GH release.

Animals↗
PubMedDate not supplied

[Growth hormone releasing hormone. Review].

Growth hormone-releasing hormone was isolated 1982 from human pancreatic tumours. They were found to consist of three peptides (GHRH1-44, GHRH1-40, GHRH1-37) which in vivo and in vitro were specific stimulators of pituitary growth hormone secretion. These tumor-derived GHRHs were demonstrated to be identical to human hypothalamic GHRHs. Extrahypothalamic GHRH is present in some brain regions and in the gastrointestinal tract. Circulating GHRH is detectable in human plasma, but little is known about its function. Above all binding of GHRH to a specific receptor stimulates growth hormone secretion through formation of cyclic AMP. GHRH secretion is modulated by somatostatin, the somatomedins and growth hormone itself. Following single injection of GHRH1-44 i.v. the equilibration half-time is 1.0 +/- 0.2 min and elimination half-time is 6.8 +/- 1.2 min. Maximal growth hormone response is achieved after injection of 1 microgram/kg GHRH. Using higher GHRH-doses growth hormone can be stimulated via subcutaneous or intranasal application. A single i.v. GHRH-test is not sufficient to prove a pituitary defect since growth hormone can be stimulated following repetitive injections in some cases. About 50% of patients with growth hormone deficiency have a hypothalamic defect of GHRH release. In some of these patients GHRH s.c. can promote linear growth to the same degree as growth hormone treatment.

Body Height↗
PubMed2002

Differential regulation of pituitary hormone secretion and gene expression by thyrotropin-releasing hormone. A role for mitogen-activated protein kinase signaling cascade in rat pituitary GH3 cells.

We examined the possible involvement of mitogen-activated protein (MAP) kinase activation in the secretory process and gene expression of prolactin and growth hormone. Thyrotropin-releasing hormone (TRH) rapidly stimulated the secretion of both prolactin and growth hormone from GH3 cells. Secretion induced by TRH was not inhibited by 50 microM PD098059, but was completely inhibited by 1 microM wortmannin and 10 microM KN93, suggesting that MAP kinase does not mediate the secretory process. Stimulation of GH3 cells with TRH significantly increased the mRNA level of prolactin, whereas expression of growth hormone mRNA was largely attenuated. The increase in prolactin mRNA stimulated by TRH was inhibited by addition of PD098059, and the decrease in growth hormone mRNA was also inhibited by PD098059. Transfection of the cells with a pFC-MEKK vector (a constitutively active MAP kinase kinase kinase), significantly increased the synthesis of prolactin and decreased the synthesis of growth hormone. These data taken together indicate that MAP kinase mediates TRH-induced regulation of prolactin and growth hormone gene expression. Reporter gene assays showed that prolactin promoter activity was increased by TRH and was completely inhibited by addition of PD098059, but that the promoter activity of growth hormone was unchanged by TRH. These results suggest that TRH stimulates both prolactin and growth hormone secretion, but that the gene expressions of prolactin and growth hormone are differentially regulated by TRH and are mediated by different mechanisms.

Animals↗
PubMed1991

Plasma growth hormone (GH)-releasing hormone levels in patients with lung carcinoma.

OBJECTIVE: The aim was to investigate the serum levels of growth hormone releasing hormone and GH in patients with lung carcinoma. DESIGN After an overnight fast a plasma sample was collected for determination of growth hormone releasing hormone and GH. PATIENTS: The investigation was performed in 28 patients with non small cell lung carcinoma, in 44 patients with small cell lung carcinoma, and 10 patients with non malignant lung disease. A group of 37 normal subjects served as control. MEASUREMENTS: Growth hormone releasing hormone and GH were determined by radioimmunoassay. RESULTS: Patients with small cell lung carcinoma showed higher plasma growth hormone releasing hormone levels (49 +/- 9.4 ng/l) than control subjects (16.3 +/- 2.1 ng/l; P less than 0.05), patients with non small cell lung carcinoma (23.9 +/- 8.8 ng/l; P less than 0.05), and patients with non malignant lung disease (12.7 +/- 5.5; P less than 0.05). Basal GH level was lower than 5 micrograms/l in all patients except five patients with small cell lung carcinoma and one patient with non small cell lung carcinoma. CONCLUSIONS: The higher plasma growth hormone releasing hormone levels in patients with small cell lung carcinoma compared to normal controls and patients with non small cell lung carcinoma and patients with non malignant lung disease, confirm the frequent neuroendocrine activity of this particular tumour.

Adult↗
PubMed1989

Pituitary immediate release pools of growth hormone and prolactin are preferentially refilled by new rather than stored hormone.

Pituitary stores of rat GH (rGH) and PRL (rPRL) are divisible into immediately releasable and more stable compartments representing either compartmentalized hormone within individual cells of a homogeneous population or responses of specialized cell subsets in a functionally heterogeneous population. In addition, newly synthesized rGH and rPRL can be processed either into intracellular storage or toward direct release. Fractional assignment of new hormone to these two paths can be influenced in the somatotroph by GHRH and may also represent either intracellular processes or functional heterogeneity of cells. We investigated the source, newly synthesized or stored, of hormone refilling the somatotroph and lactotroph immediately releasable pools (IRP) after their discharge by 21 mM potassium ion, 1 mM (Bu)2cAMP, 3 nM human GHRH-44, or 3 microM prostaglandin E1. Experiments were performed using perifused pituitary fragments exposed sequentially to [14C]- and [3H]leucine in association with stimulation by two 30-min pulses of the same secretagogue. Therefore, only [14C]hormone was available for release by the first stimulus, whereas both [14C]- and [3H]hormone were available for release by the second stimulus. Analysis was by specific immunoprecipitation. The first episode of stored [14C]rGH release exceeded the second episode of stored [14C]rGH release in response to each secretagogue. However, release of newly synthesized [3H]rGH in response to the second episode of stimulation exceeded the simultaneous release of stored [14C]rGH while matching or exceeding the [14C]rGH release that had occurred in the same experiment in response to the first episode of stimulation. Refilling both GH and PRL IRP stores drew primarily upon newly synthesized hormone, but with different secretagogue-specific patterns. These data confirm differential handling of new and stored rGH and rPRL within the pituitary. They are consistent with either (1) the enhanced shunting of newly synthesized hormone to IRPs within cells that are capable of compartmentalized intracellular hormone storage, or (2) the relatively complete discharge of a subset of somatotrophs and lactotrophs that are specialized to deliver pulsed hormone release, after which they are refilled by newly synthesized hormone.

Alprostadil↗
PubMed1988

c-erbA protooncogenes mediate thyroid hormone-dependent and independent regulation of the rat growth hormone and prolactin genes.

Regulation of gene expression by the thyroid hormones is thought to be mediated by a nuclear-associated receptor found in a wide variety of cells and tissues. Cellular homologues of the avian erythroblastosis virus oncogene, v-erbA, encode proteins which bind thyroid hormone with similar affinities as thyroid hormone receptors. However, it has not been shown that any of the c-erbA proteins can function as receptor and modulate thyroid hormone responsive genes. In this study, using transient expression of chimeric reporter constructs, we document that the chick fibroblast c-erbA-alpha and the human placental c-erbA-beta modulate cis-acting regulatory sequences of two thyroid hormone responsive genes; rat GH and PRL. From these results we conclude: 1) in a receptor deficient cell line (235-1) both c-erbA subtypes act as hormone-dependent modulators of PRL gene expression and hence function as thyroid hormone receptors, 2) in two different receptor containing cell lines (GH4C1 and GH1), both c-erbA proteins act in a hormone-independent fashion to regulate PRL and GH expression. This suggests that events other than ligand binding can result in formation of a c-erbA protein that modulates transcription of thyroid hormone responsive genes, 3) no qualitative functional differences were detected between alpha- and beta-c-erbA subtypes, and 4) depending on the cell-type, L-T3 acts through its endogenous receptor to stimulate (GH4C1) or suppress (GH1) expression of a chimeric PRL construct. In these cells, c-erbA expression results in the same positive or negative response as the endogenous receptor except that the response occurs in the absence of hormone. These results suggest that the endogenous receptor and the c-erbAs act by augmenting the effect of transcription factors which can positively or negatively control gene expression.

Affinity Labels↗
PubMed1982

Selectivity of melatonin pituitary inhibition for luteinizing hormone-releasing hormone.

The pineal indole melatonin suppresses the neonatal rat luteinizing hormone (LH) and follicle-stimulating hormone (FSH) responses to LH-releasing hormone (LHRH), as shown in previous studies from this laboratory. We show in this study that the melatonin inhibition is a selective effect and is not due to general inhibition of pituitary function. The effects of the indole on the responses to thyrotropin-releasing hormone (TRH) and somatostatin (SRIF) and on basal pituitary hormone secretion were examined with cells in culture. Neonatal rat anterior pituitary cells dissociated with collagenase and hyaluronidase were cultured overnight and distributed to 35-mm dishes at the time of use. For examination of melatonin effects on the response to releasing hormones, the cells were incubated for 3 h in control medium or medium containing LHRH (10-9-10-6 M), TRH (10-10-10-6 M), or SRIF (10-9-10-6 M), either alone or in the presence of melatonin (10-8 or 10-6 M). For examination of basal hormone secretion, the cells were incubated for 1.5, 3, 6, 15, or 24 h in either medium alone or medium containing melatonin (10-6 M). Medium and cell lysate concentrations of LH, FSH, thyroid-stimulating hormone (TSh), prolactin (PRL) and growth hormone (GH) were determined by double antibody RIA. As previously, melatonin (10-8 M) significantly suppressed LH and FSH release by all concentrations of LHRH. This concentration of the indole produced maximal suppression of both LH and FSH responses to LHRH. By contrast, melatonin at a 100-fold greater concentration (10-6 M) had no effect on TRH stimulation of TSH or PRL release or on SRIF inhibition of GH release. Similarly, melatonin had no effect on basal release of TSH, PRL, or GH at the times examined. These findings show that melatonin inhibition of the gonadotroph response to LHRH is a selective effect.

Animals↗
PubMed1991

Serum glucose and free fatty acids modulate growth hormone and luteinizing hormone secretion in the pig.

Two experiments were conducted to determine the effect of free fatty acids (FFA) and glucose treatment on growth hormone (GH) and luteinizing hormone secretion in the pig. In Experiment (Exp) 1, 15 prepuberal gilts received an intravenous infusion of FFA (n = 5; 3 ml of 10% Liposyn II/kg), glucose (n = 5; 1 g/kg), or saline (n = 5; 3 ml of 0.9%/kg). Jugular blood samples were collected every 15 min for 2 hr before and 3 hr after intravenous infusion of saline, FFA, and glucose. Synthetic [Ala15]-h growth hormone-releasing factor-(1-29)NH2 (1 microgram/kg) and gonadotropin-releasing hormone (0.2 micrograms/kg) were administered 30 min after infusion (Time 0 = infusion). In Exp 2, eight prepuberal gilts received either FFA (n = 4) or saline (n = 4) as described in Exp 1, except that treatments were given every hour ove a 10-hr period. Blood samples were collected every 15 min from 1 hr before to 10 hr after the start of FFA or saline infusion. In Exp 1, the peak GH response to growth hormone-releasing factor was delayed by 45 min (P less than 0.01) by glucose treatment and suppressed (P less than 0.01) by FFA treatment. The luteinizing hormone response to gonadotroph-releasing hormone was suppressed (P less than 0.03) by glucose and enhanced (P less than 0.03) by FFA. In Exp 2, the number of GH pulses was increased (P less than 0.05) by FFA infusion and GH concentrations were positively correlated (r = 0.58, P less than 0.0003) with FFA concentrations, while luteinizing hormone pulse amplitude was greater (P less than 0.01) in FFA gilts than in saline gilts. These results indicate that FFA are more effective modulators of GH secretion than acute hyperglycemia, while metabolic status can alter pituitary responsiveness to gonadotropin-releasing hormone.

Animals↗
PubMed1995

Interdependence of corticosterone and thyroid hormones in larval toads (Bufo boreas). I. Thyroid hormone-dependent and independent effects of corticosterone on growth and development.

In a previous study (Hayes et al. [1993] J. Exp. Zool., 266:206-215), we demonstrated that exogenous corticosterone (B) inhibited growth, and had varied effects on development and metamorphosis in the toad (Bufo boreas). The current study determined the relation between the actions of B and thyroid hormones on body growth (length and weight), tail growth and reduction (length and height), rear leg growth and differentiation, and foreleg emergence (FLE). Thiourea (Thio; a goitrogen) and metyrapone (MTP; a glucocorticoid synthesis inhibitor) were used to determine the role of endogenous hormones in growth and development. These inhibitors were also used in various combinations with the thyroid hormones, thyroxine (T4) and triiodothyronine (T3), to determine the extent to which B's actions depend on the thyroid hormones. B was ineffective at inducing tail reduction (length and height) in the presence of Thio, but B enhanced the effects of both thyroid hormones, suggesting that the actions of B on the tail were dependent on thyroid hormones. B inhibited body growth even in the presence of Thio, but did not enhance thyroid hormone's inhibition of growth. B alone stimulated foreleg emergence (FLE) and enhanced thyroid hormone's activity on FLE when B and the thyroid hormones were given in combination, but did not induce FLE in the presence of Thio. B stimulated rear leg development, but not in the presence of Thio, suggesting that this effect was due to interactions with thyroid hormones. Furthermore, MTP antagonized the stimulatory effect of T4 on rear leg development, suggesting that endogenous B also interacted with exogenous thyroid hormones.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1979

Transport of steroid hormones through the rat blood-brain barrier. Primary role of albumin-bound hormone.

These studies were undertaken to investigate (a) the permeability properties of the blood-brain barrier (BBB) to the major gonadal and adrenal steroid hormones, and (b) the role of the binding proteins of plasma (albumin and specific globulins) in the regulation of BBB steroid hormone transport. The permeability of the BBB to [(3)H]-labeled progesterone, testosterone, estradiol, corticosterone, aldosterone, and cortisol, was measured relative to [(14)C]butanol, a freely diffusable reference, in the barbiturate anesthetized rat using a tissue sampling-single injection technique. The isotopes were rapidly injected in a 200-mul bolus of Ringer's solution (0.1 g/dl albumin) via the common carotid artery and the percent extraction of unidirectional influx of hormone was determined after a single pass through brain: progesterone, 83+/-4%; testosterone, 85+/-1%; estradiol, 83+/-3%; corticosterone, 39+/-2%; aldosterone, 3.5+/-0.8%; and cortisol, 1.4+/-0.3%. The selective permeability of the BBB was inversely related to the number of hydrogen bonds each steroid formed in aqueous solution and directly related to the respective 1-octanol/Ringer's partition coefficient. When the bolus injection was 67% human serum, >95% of the labeled steroid was bound as determined by equilibrium dialysis. However, the influx of the steroids through the BBB was inhibited by human serum to a much less extent than would be expected if only the free (dialyzable) hormone was transported; progesterone, estradiol, testosterone, and corticosterone transport was inhibited 18, 47, 70, and 85% respectively, or in proportion to the steroid binding to plasma globulins. Rat serum (67%) only inhibited the transport of these four hormones, 0, 13, 12, and 69%, respectively, reflecting the absence of a sex hormone-binding globulin in rat plasma. However, neonatal rat serum (67%) inhibited progesterone, testosterone, and estradiol transport 0, 0, and 91%, respectively, consistent with the presence of an estradiol-binding protein in neonatal rat serum. The binding of steroid hormone to bovine albumin in vitro (as determined by equilibrium dialysis) was compared to albumin binding in vivo (as determined by the single injection technique). The ratio of apparent dissociation constant in vivo, K(D)(app), to the in vitro K(D) was: >>200 for progesterone, >200 for testosterone, 120 for estradiol, and 7.7 for corticosterone. Assuming the steady-state condition, the K(D)(app)/K(D) was found to be proportional to the BBB permeability for each steroid. These data demonstrate (a) the selective permeability properties of the BBB to the major steroid hormones is proportional to the tendency of the steroid to partition in a polar lipid phase and is inversely related to the number of hydrogen bond-forming functional groups on the steroid nucleus; (b) the presence of albumin in serum may bind considerable quantities of steroid hormone, but exerts little inhibitory effects on the transport of steroids into brain, whereas globulin-bound hormone does not appear to be transported into brain to a significant extent. Therefore, the hormone fraction in plasma that is available for transport into brain is not restricted to the free (dialyzable) fraction, but includes the larger albumin-bound moiety.

Aldosterone↗