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PubMed1985

Spontaneous proliferative lesions of the adrenal medulla in aging Long-Evans rats. Comparison to PC12 cells, small granule-containing cells, and human adrenal medullary hyperplasia.

Aging rats of the Long-Evans strain spontaneously develop diffuse and nodular hyperplasia of the adrenal medulla in association with other abnormalities commonly encountered in human multiple endocrine neoplasia syndromes. The cells which comprise the adrenal nodules resemble those in the parent tumor of the rat PC12 pheochromocytoma cell line in that they show varying degrees of spontaneous or nerve growth factor-induced neurite outgrowth in culture and they contain little or no epinephrine. In addition, cells from at least some of the nodules contain immunoreactive neurotensin and neuropeptide-Y, which are also found in PC12 cells. There are a number of striking resemblances between the cells in adrenal nodules and the small granule-containing cells in the normal rodent adrenal. The findings suggest that spontaneous rat adrenal medullary nodules and PC12 cells might be derived from small granule-containing cells, or that cells within the nodules might regain properties of immature chromaffin cells and acquire characteristics of small granule-containing cells and of PC12 cells in the course of neoplastic progression. They further suggest a possible relationship between proliferative capacity and neurotransmitter phenotype in the adult rat adrenal medulla. By virtue of their sparse epinephrine content and their small granules, the cells in adrenal medullary nodules of Long-Evans rats differ from those in adrenal medullary nodules of humans with multiple endocrine neoplasia syndromes.

Acetylcholinesterase↗
PubMed1998

Class III beta-tubulin isotype (beta III) in the adrenal medulla: I. Localization in the developing human adrenal medulla.

BACKGROUND: The class III beta-tubulin isotype (beta III) is present in neurons of the central and peripheral nervous systems at the earliest stages of morphological differentiation (Easter et al., J Neurosci 13:285-299, 1993; Katsetos et al., J Neuropathol Exp Neurol 52:655-666, 1993). The localization of this protein by immunohistochemistry in the different cell types of the developing human adrenal medulla is described. METHODS: A mouse monoclonal antibody, TuJ1, was used to localize beta III in formalin-fixed, paraffin-embedded sections from 18 human fetal and adult adrenal glands. Tissue sections were also studied with rabbit antisera recognizing either S-100 protein or glial fibrillary acidic protein (GFAP). RESULTS: In the developing human adrenal medulla, beta III immunoreactivity was maximal in migrating sympathoadrenal neuroblasts/immature neurons through the end of the second trimester. Clusters of beta III-positive migrating cells, focally forming Homer Wright rosettes, could be identified in a gradient of adrenocortical invasion, i.e., through the permanent cortex and within sinusoids of the fetal cortex en route to the medulla. Outside the adrenal gland, strong beta III staining was observed in peripheral nerve bundles, sympathetic ganglia, and paraganglia at various developmental stages. In adrenal glands from 23 weeks of gestation on, and throughout adult life, all ganglion cells were beta III immunoreactive. In contrast, not all chromaffin cells exhibited beta III staining, but when present, the staining was finely granular. Sustentacular and satellite cells, adrenocortical cells and other mesenchymal elements were betaIII-negative. In sections of fetal and adult adrenal glands, S-100 protein had a sustentacular localization. No GFAP staining was present in sustentacular cells from either fetal or adult adrenals. CONCLUSIONS: In the developing human adrenal medulla, there is a peak of beta III expression during the active wave of migration of sympathetic neuroblasts. In the mature medulla, beta III is invariably present in adrenergic neurons. However, not all chromaffin-like cells express beta III, suggesting that the presence or absence of this protein identifies two subpopulations of chromaffin cells.

Adrenal Medulla↗
PubMed2003

Adrenal neuropeptides: regulation and interaction with ACTH and other adrenal regulators.

It is now well accepted that both the cortex and medulla of the mammalian adrenal gland receive a rich innervation. Many different transmitter substances have been identified in nerves supplying both cortex and medulla and, as well as catecholamines, a wide range of neuropeptides has been found in the adrenal gland. There have been several studies on the affects of age, sodium intake, stress, ACTH, and splanchnic nerve activity on the regulation of adrenal neuropeptide content. There is evidence that the abundance of each of these peptides is actively regulated. Although there have been many studies addressing the individual actions of various neurotransmitters on steroid secretion, adrenal blood flow, and adrenal growth, few have attempted to determine the nature of any interaction between neurotransmitters and the classical adrenal stimulants. There are, however, some significant interactions, particularly in the regulation of zona glomerulosa function. This review necessarily focuses on vasoactive intestinal peptide (VIP) and neuropeptide Y (NPY), as these are the most abundant transmitter peptides in the adrenal gland and the majority of studies have investigated their regulation and actions. However, substance P, calcitonin gene-related peptide (CGRP), neurotensin, and the enkephalins are included where appropriate. Finally, it has been suggested that certain neurotransmitters, particularly VIP, may interact with classical hormone receptors in the adrenal, notably the ACTH receptor. This review attempts to evaluate our current state of knowledge in each of these areas.

Adrenal Glands↗
PubMed2000

Expression of stanniocalcin in zona glomerulosa and medulla of normal human adrenal glands, and some adrenal tumors and cell lines.

Stanniocalcin (STC) is a calcium (Ca)-regulating hormone that was originally discovered in the fish Stannius body, which is a unique endocrine organ. Hypercalcemia increases STC secretion, which inhibits Ca uptake by the gills and normalizes serum Ca level. In this study we investigated the STC expression in human normal and abnormal adrenal cells. Immunohistochemistry using monoclonal antibody against STC revealed specific staining in zona glomerulosa and medulla of normal human adrenal glands. STC was also detected in human adrenal tumors, such as pheochromocytoma, differentiated neuroblastoma, and aldosterone-producing adenoma, and cultured adrenal tumor cells (rat pheochromocytoma PC-12 cells and human neuroblastoma NB-1 cells). However, undifferentiated human adrenal neuroblastoma was negative for STC staining. Reverse transcription polymerase chain reaction demonstrated STC mRNA expression in cultured PC-12 cells and NB-1 cells. Following several studies indicating that zona glomerulosa cells of adrenal glands express neuroendocrine properties, STC expression in normal and abnormal adrenal cells provides additional evidence to support the neuroendocrine differentiation of these cells. In conclusion, STC may be useful as a new cell marker of adrenal glands under physiological and pathological conditions.

Adrenal Medulla↗
PubMed2006

A primary adrenal non-Hodgkin's lymphoma presenting as an incidental adrenal mass.

The primary adrenal localization of a non-Hodgkin's lymphoma (NHL) is a rare event. We report the case of a 70-yr-old woman, who was admitted at our Institute for a hormonal evaluation after the incidental discovery of a right adrenal mass during ultrasonography (US) performed for cardiovascular disease. At the physical examination, no sign of adrenal hyperfunction was present. She showed only an androgenetic alopecia and her blood pressure was 180/70 mm Hg, with an arrhythmic heart rate of 100 beats/min. No alterations in hormonal and biochemical data were observed. US studies showed a right adrenal mass (major diameter 16 mm), and an abdominal computed tomography (CT) scan confirmed this solid lesion (major diameter 15 mm) with a high density. [75Se] methylnorcholesterol adrenal scintigraphy exhibited a normal symmetrical radiotracer uptake. After 8 months of follow-up, an abdominal CT scan demonstrated a significant increase of the right adrenal mass (major diameter: 40 mm), with a solid tissue density and enhancement after i.v. contrast. [75Se] methylnorcholesterol adrenal scintigraphy showed an absent uptake on the right side versus the contralateral side. The hematological, hormonal and radiological evaluation did not reveal any sign of malignancy. Owing to the mass enlargement and the modification of scintigraphic pattern, the patient underwent unilateral adrenalectomy. Histological examination revealed a primary diffuse large B-cell NHL (REAL classification) of the adrenal gland. After surgery, she underwent a combined polychemotherapy (cyclophospamide, adriamycin, vincristine and prednisone) and subsequently one cycle of radiotherapy. At present, the patient is in good conditions and there are no signs or symptoms of recurrent disease.

Adrenal Gland Neoplasms↗
PubMed1997

Characterization of the adrenal cytochrome P450C17 in the hamster, a small animal model for the study of adrenal dehydroepiandrosterone biosynthesis.

The hamster, like the human produces cortisol as its major glucocorticoid, rather than corticosterone, typical of most enzyme rodents. It is not known, however, if the hamster cytochrome P450C17 (P450C17), a key enzyme for cortisol formation, also exhibits 17,20-lyase activity and if it catalyzes the formation of dehydroepiandrosterone (DHEA) at the adrenal level. To study this, we isolated the cDNA of P450C17 from a hamster adrenal library. This cDNA was sequenced and was found to have an open reading frame for a protein of 511 amino acids, as compared to the human P450C17, which contains 508 amino acids. The hamster P450C17 cDNA, in the coding region, is 76% homologous with the human P450C17 cDNA. The cDNA was then cloned in the expression vector pSV-SPORT 1, which was transiently transfected into COS 1 cells. The transfected cells were used for temporal studies on the transformation of radiolabeled C21-delta5- and C21-delta4-precursors. When transfected cells were incubated with [14C]pregnenolone, rapid formation of [14C]DHEA occurred. The intermediate 17alpha-hydroxypregnenolone accumulated initially with subsequent metabolism to DHEA. Likewise, when incubated with C21-delta4-steroids, [14C]progesterone and [3H]17alpha-hydroxyprogesterone, the 17,20-lyase product androstenedione was produced efficiently. In these studies, with respect to the delta5 pathway, the expressed hamster P450C17 gave similar results to bovine P450C17 cDNA inserted in the same expression vector. However, in contrast to the bovine enzyme, which converted low amounts of progesterone to androstenedione, the expressed hamster P450C17 enzyme showed an active metabolism via the delta4 pathway. Northern blot analysis, using the complete alpha-32P labeled hamster P450C17 cDNA as the probe, demonstrated a strong presence of P450C17 mRNA in hamster adrenals, a weaker presence in testes and ovaries, and no detectable species in brain, mesentery, and kidney. Immunoblotting analysis using an anti-rat P450C17 antibody demonstrated the presence of P450C17 protein in hamster adrenals, testes, and ovaries. Hamster adrenal cell suspensions and microsomal preparations were used to demonstrate the biosynthesis of [14C]17alpha-hydroxypregnenolone and [14C]DHEA from [14C]pregnenolone; both metabolites were formed during incubations. However, the ratio of [14C]DHEA/[14C]17alpha-hydroxypregnenolone was much lower in adrenal cells than in transfected COS 1 cells, indicating the presence of putative factors in hamster adrenal cells, favoring the 17alpha-hydroxylase activity rather than that of the 17,20-lyase. In conclusion, these studies demonstrate that the hamster adrenal is both a DHEA and a cortisol producer, and, therefore, this animal could be a suitable small animal model for the study of the role of DHEA in relation to human biochemistry and physiology.

Adrenal Glands↗
PubMedDate not supplied

Human chorionic gonadotropin does not alter patterns of adrenal androgen secretion in primary human adrenal reticularis and fasciculata cell culture.

OBJECTIVE: Controversy surrounds the role of the ovary in maintaining postmenopausal androgen levels. Some postulate that aging ovaries are endocrinologically senescent and that menopausal levels of luteinizing hormone drive the adrenal cortex to secrete increasing amounts of dehydroepiandrosterone (DHEA) and dehydroepiandrosterone sulfate (DHEAS) as prohormones for subsequent peripheral bioconversion to maintain menopausal testosterone levels. We hypothesized that human chorionic gonadotropin (hCG), acting as an luteinizing hormone analog, would thus augment adrenal androgen secretion from primary human adrenocortical zona reticularis and zona fasciculata cell cultures. DESIGN: Human adrenal glands, obtained from a local organ donation program, were separated microscopically into reticularis and fasciculata zones and were cultured to confluence in serum-supplemented media, followed by a further incubation in defined media. They were then exposed to 24 hours of varying hCG doses, followed by an incubation with defined media and pregnenolone. Supernatants were assayed for adrenal androgens and cortisol. Data were expressed as the molar ratio of (DHEA+ DHEAS)/cortisol and the molar ratio of DHEA/DHEAS. For each of the four runs, mean molar ratios were compared by analysis of variance. RESULTS: For each of the four runs, the molar ratio was increased 17- to 157-fold in the reticularis compared with the fasciculata cells, indicating efficient zonal separation. Addition of hCG did not alter the molar ratios of adrenal androgens to cortisol or DHEA/DHEAS for either cell type. CONCLUSIONS: Addition of hCG to human adrenal reticularis or fasciculata cells does not seem to change the pattern of secretion of adrenal androgens or cortisol. It is thus unlikely that luteinizing hormone plays a significant role as an adrenal androgen secretagogue, at least with short-term exposure.

Adrenal Cortex↗
PubMed2002

Capsaicin-sensitive adrenal sensory fibers participate in compensatory adrenal growth in rats.

Compensatory adrenal growth, in which one gland undergoes hyperplasia after removal of the other, is mediated by a neural reflex. In the present studies, a method employing capsaicin to selectively remove adrenal sensory fibers was developed and applied to determine whether adrenal capsaicin-sensitive fibers participate in compensatory adrenal growth. The splanchnic nerves of anesthetized male rats were treated with capsaicin or vehicle. Capsaicin treatment selectively removed adrenal calcitonin gene-related peptide-positive fibers. One week after drug treatment, rats underwent left adrenalectomy or sham surgery and recovered for 5 days. Capsaicin treatment bilaterally or to the left splanchnic nerve alone (i.e., the afferent nerve in the reflex) impaired compensatory adrenal growth at 5 days compared with vehicle controls, whereas capsaicin treatment to the right splanchnic nerve alone did not affect growth. Moreover, left adrenalectomy induced c-Fos immunolabeling in ipsilateral dorsal spinal cord that was prevented by capsaicin treatment. These data suggest that adrenal capsaicin-sensitive afferent nerves participate in compensatory adrenal growth and that this effect is primarily on the afferent limb of the reflex.

Adaptation, Physiological↗
PubMed2004

Adrenal aldosterone biosynthesis is elevated in a model of chronic renal failure--role of local adrenal renin-angiotensin system.

BACKGROUND: Aldosterone seems to play a role in the development of chronic renal failure and proteinuria. We investigated the adrenal aldosterone production and the adrenal renin-angiotensin system (RAS) in rats with 5/6 nephrectomy with and without spironolactone treatment. METHODS: Sprague-Dawley rats underwent 5/6, 4/6 nephrectomy, heminephrectomy and sham operation. After 1 and 4 weeks creatinine clearance, urinary protein excretion, plasma aldosterone concentration, and plasma renin activity were measured. In adrenals mRNA expression of aldosterone synthase (CYP11B2) and genes of the RAS were measured. RESULTS: Creatinine clearance was significantly decreased and proteinuria significantly elevated in 5/6 nephrectomy. Treatment with spironolactone significantly reduced proteinuria after 8 but not after 30 days. With reduction of renal mass, renal renin mRNA and plasma renin activity were reduced significantly. In early 5/6 nephrectomy plasma aldosterone concentration was increased and in parallel adrenal CYP11B2 mRNA was increased significantly. Both were further augmented by spironolactone. Adrenal renin was up-regulated in 5/6 nephrectomy and further stimulated with spironolactone, possibly serving as a stimulus for the adrenal aldosterone synthesis. CONCLUSION: In early chronic renal failure after 5/6 nephrectomy adrenal aldosterone production is elevated despite a marked decrease of plasma renin activity. An up-regulated adrenal RAS may contribute to the observed increase in aldosterone.

Adrenal Glands↗
PubMed1972

Metabolism of adrenal cholesterol in man. II. In vitro studies including a comparison of adrenal cholesterol synthesis with the synthesis of the clucocorticosteroid hormones.

The synthesis of adrenal cholesterol, its esterification and the synthesis of the glucocorticosteroid hormones were studied in vitro on human adrenal tissue. It was found that the synthesis of adrenal cholesterol may normally be small in the zona "fasciculata," particularly when compared with the synthesis of the glucocorticosteroid hormones, that it is several times higher in the zona "reticularis" where esterified cholesterol is less abundant, and that under ACTH stimulation it increases strikingly and proportionally to the degree of esterified adrenal cholesterol depletion. ON THE OTHER HAND, THE RELATIVE RATE OF ESTERIFICATION AS WELL AS THE CONCENTRATION OF FREE ADRENAL CHOLESTEROL ARE REMARKABLY STABLE: they do not differ according to the adrenal zonation and are unaffected by ACTH. Furthermore, from a qualitative point of view, the relative proportions of Delta(1) and Delta(2) cholesteryl esters formed in situ are similar to those anticipated from their relative concentrations, suggesting that the characteristic fatty acid distribution of the adrenal cholesteryl esters results from an in situ esterification rather than from a selective uptake of the plasma cholesteryl esters. Besides, the in vitro esterification reveals a propensity to the formation of the most unsaturated cholesteryl esters. Regarding hydrocortisone and corticosterone, their synthesis tends to be more elevated in the zona "fasciculata." Despite its higher cholesterol concentration the zona "fasciculata" should not therefore be viewed as a quiescent functional complement to the zona "reticularis" and the cortical distribution of glucocorticosteroid hormone synthesis is quite distinct from that of adrenal cholesterol synthesis.

Acetates↗
PubMed2003

GATA-6 is expressed in the human adrenal and regulates transcription of genes required for adrenal androgen biosynthesis.

GATA-6 and GATA-4 are members of a family of transcription factors (GATA 1-6) that share conserved zinc-finger DNA binding domains. Using semiquantitative RT-PCR, we found that the human adrenal expresses mRNA for GATA-6 but not GATA-4. A recent study showed GATA-6 expression in the adrenal reticularis, the source of adrenal androgens. To investigate the role of GATA-6 in regulation of adrenal cell steroidogenesis, luciferase reporter constructs containing the 5'-flanking DNA from steroidogenic acute regulatory protein, cholesterol side-chain cleavage (CYP11A), 17alpha-hydroxylase (CYP17), and dehydroepiandrosterone-sulfotransferase (SULT2A1) were cotransfected with an expression vector containing GATA-6 into adrenal NCI-H295R cells and nonsteroidogenic HEK293 cells. All promoter/reporter constructs were increased by GATA-6 in the adrenal model. However, in the HEK293 cells only SULT2A1 reporter activity was increased by GATA-6. One key difference between H295R and HEK293 cell lines is the differential expression of steroidogenic factor 1 (SF1). Transfection of HEK293 cells with both GATA-6 and SF1 significantly increased transcriptional activation of all reporter constructs above the effect of GATA-6 or SF1 alone. To determine whether the action of GATA-6 required SF1, we transfected HEK293 cells with each promoter construct plus and minus GATA-6, SF1, and/or the orphan nuclear repressor DAX1. DAX1 opposed SF1-activated transcription of many genes and abolished the GATA-6/SF1 ability to increase reporter activity. These results suggest that the adrenal uses GATA-6 to enhance transcription of steroid-metabolizing enzymes needed to produce dehydroepiandrosterone sulfate. Additionally, GATA-6 works in synergy with SF1 to maximally increase expression of enzymes needed to produce adrenal androgens.

Adrenal Glands↗
PubMed2006

Expression and externalization of annexin 1 in the adrenal gland: structure and function of the adrenal gland in annexin 1-null mutant mice.

Annexin 1 (ANXA1) is a member of the annexin family of phospholipid- and calcium-binding proteins with a well demonstrated role in early delayed (30 min to 3 h) inhibitory feedback of glucocorticoids in the hypothalamus and pituitary gland. This study used adrenal gland tissue from ANXA1-null transgenic mice, in which a beta-galactosidase (beta-Gal) reporter gene was controlled by the ANXA1 promoter, and wild-type control mice to explore the potential role of ANXA1 in adrenal function. RT-PCR and Western blotting revealed strong expression of ANXA1 mRNA and protein in the adrenal gland. Immunofluorescence labeling of ANXA1 in wild-type and beta-Gal expression in ANXA1-null adrenals localized intense staining in the outer perimeter cell layers. Immunogold electron microscopy identified cytoplasmic and nuclear ANXA1 labeling in outer cortical cells and capsular cells. Exposure of adrenal segments in vitro to dexamethasone (0.1 mum, 3 h) caused an increase in the amount of ANXA1 in the intracellular compartment and attached to the surface of the cells. The N-terminal peptide ANXA1(Ac2-26) inhibited corticosterone release. Corticosterone release was significantly greater from ANXA1-null adrenal cells compared with wild type in response to ACTH (10 pm to 5 nm). In contrast, basal and ACTH-stimulated aldosterone release from ANXA1-null adrenal cells was not different from wild type. Morphometry studies demonstrated that ANXA1 null adrenal glands were smaller than wild-type, and the cortical/medullary area ratio was significantly reduced. These results suggest ANXA1 is a regulator of adrenocortical size and corticosterone secretion.

Adrenal Glands↗
PubMed1989

An endogenous digitalis-like factor derived from the adrenal gland: studies of adrenal tissue from various sources.

We have previously reported that the adrenal gland is the probable origin of the digitalis-like immunoreactive material (DLI) present in the plasma of rats and other species which have never received cardiac glycoside drugs. The present study demonstrates that adrenal glands removed from rats and then chopped release an immunoreactive digitalis-like material into a serum-free minimal incubation medium. HPLC studies indicated that this immunoreactivity was not homogeneous. Since such material may be a mammalian steroidal ligand for the glycoside receptor on the sodium pump, we investigated whether release of this material could be inhibited by antagonizing the conversion of cholesterol to pregnenolone through the addition of aminoglutethimide (AG) to the incubation medium. Our observations indicate that this manipulation successfully inhibited pregnenolone production during both of our 2-h serial incubation periods. However, in neither incubation period was AG able to inhibit the release of DLI into the medium; rather, during the first 2-h period, the release of this material was increased in the presence of AG compared to that in controls. We attempted to determine whether DLI was of adrenocortical or medullary origin. Extracts of whole beef adrenal gland, beef cortex, whole rat adrenal gland, and whole dog adrenal gland diluted in parallel in RIA, suggesting that the assay detected the same or similar material in each tissue sample. Medullary and cortical tissue samples were dissected from slices of fresh beef adrenals and extracted for assay. These data indicated that the cortex was the primary source of endogenous digitalis-like material. Efforts to enhance release of this material from the cortex of intact rats was performed by exposing animals to ether stress. After ether stress, the plasma concentration of digitalis-like material was lower than that in controls. Finally, extracts of incubation medium from chopped adrenal glands indicate that this medium possesses the ability to inhibit the binding of radiolabeled ouabain to human erythrocytes, suggesting that adrenal glands release material that has the ability to be recognized by both antidigoxin antibodies and the ouabain-binding site of erythrocyte membrane Na+,K+-ATPase.

Adrenal Glands↗
PubMed1976

Gonadotropin output in congenital adrenal hyperplasia before and after adrenal suppression.

Basal release of gonadotropin and the response to an infusion of 100 mug of synthetic luteinizing hormone releasing hormone (LRH) were studied in a teenage girl with congenital adrenal hyperplasia (CAH). The initial study was done during a period of poor adrenal suppression, and second study was done after adequate adrenal suppression was achieved. To assess adrenal function, circulating levels of adrenal steroid hormones were evaluated continuously over a 24 h period. During the period increased production of adrenal androgens, the pattern of gonadotropin release was that of a prepubertal child. After 3 months of adrenal suppression the pattern of gonadotropin secretion was similar to that of a normal girl in mid-puberty. This demonstrates the rapid change from prepubertal to pubertal gonadotropin dynamics in a teenage patient following adequate suppression of androgens from the adrenal.

17-Ketosteroids↗
PubMed1987

[Characterization of adrenal medullary opioid receptors. I. Binding of opioids to adrenal medullary opioid receptors].

We studied the binding of [3H]D-Ala2-D-Leu5-enkephalin ([3H]DADLE) and [3H] diprenorphine to crude plasma membrane fraction obtained from the bovine adrenal medulla (bovine adrenal medullary membranes) in order to characterize adrenal medullary opioid receptors. The [3H] diprenorphine binding was the highest in crude plasma membrane-mitochondrial fraction among all subcellular fractions studied. The amount of [3H] diprenorphine bound to bovine adrenal medullary membranes was proportional to the protein concentration. Association kinetics of the [3H] diprenorphine binding to bovine adrenal medullary membranes showed that the maximal binding was achieved following 8 min incubation and that the binding conformed the second-order kinetics. [3H] DADLE and [3H] diprenorphine bound to bovine adrenal medullary membranes with high affinities. The Kd and Bmax for the [3H] DADLE binding were found to be 2.9 nM and 57.5 fmole/mg protein, respectively, while those for the [3H] diprenorphine binding were 0.31 nM and 250 fmole/mg protein, respectively. Displacement studies showed that the [3H] diprenorphine binding was inhibited dose-dependently by levorphanol, dynorphin (1-13), beta-endorphin and DADLE. Levorphanol was at least 1000-fold more potent to inhibit the [3H] diprenorphine binding than dextrorphan, indicating stereospecificity of the [3H] diprenorphine binding. Na+, Li+ and K+ (100 mM) diminished the [3H] DADLE binding and enhanced [3H] diprenorphine binding. Na+ (100 mM) increased the Kd value for the [3H] DADLE binding from 2.9 nM to 14.1 nM. Mn++, Ca++ and Mg++ diminished the [3H] diprenorphine binding. Mn++ (1 mM) increased the Bmax value for the [3H] DADLE binding from 95 fmole/mg protein to 450 fmole/mg protein. These effects of Na+ and Mn++ on the [3H] diprenorphine binding were found to be dose-dependent. [3H] Diprenorphine binding to the digitonin-solubilized opioid receptor was also inhibited dose-dependently by Mn++. These results suggest that bovine adrenal medullary membranes contain high affinity and stereospecific opioid receptors and that the binding of opioids to the bovine adrenal medullary opioid receptors is influenced by cations. Binding study also revealed the presence of opioid receptors in human malignant pheochromocytoma. The Kd and Bmax of the [3H] diprenorphine binding to crude membrane fraction obtained from malignant pheochromocytoma were found to be 0.14 nM and 10.4 fmole/mg protein, respectively.

Adrenal Medulla↗
PubMed2004

The endocrinology of adrenal tuberculosis: the effects of tuberculosis on the hypothalamo-pituitary-adrenal axis and adrenocortical function.

Tuberculosis may affect many of the endocrine glands including the hypothalamus, pituitary, thyroid and adrenals. The most commonly involved endocrine organ in tuberculosis is the adrenal gland. Adrenal glands may be directly or indirectly affected by tuberculosis. Tuberculous Addison's disease is still an important cause of primary adrenocortical insufficiency particularly in the developing countries. Recent improvements in imaging techniques and modern endocrinological tests for the investigation of adrenal function have given us greater insight into the endocrinology of adrenal tuberculosis. Hypothalamo-pituitary-adrenal (HPA) axis is also involved in tuberculosis and recent findings revealed that HPA axis is activated rather than underactivated in active pulmonary tuberculosis. Activated HPA axis in tuberculosis causes increased cortisol secretion which results in a shift in the Th1/Th2 balance towards Th2. T cell dysfunction due to high cortisol and low DHEAS levels may be responsible for immunologically-mediated tissue damage in tuberculosis. In this review, recent findings concerning the adrenocortical function, radiological changes in adrenal glands and HPA axis involvement in tuberculosis are discussed.

Addison Disease↗
PubMed1996

Adrenal gland volume in major depression: relationship to basal and stimulated pituitary-adrenal cortical axis function.

We measured adrenal gland volume and both baseline and stimulated pituitary and adrenal cortical hormones in 35 unmedicated, major depressives and 35 individually matched normal control subjects. Mean adrenal volume in the depressives was significantly larger, by about 38%, than the adrenal volume of their matched controls. Basal plasma adrenocorticotropic hormone (ACTH)1-39 was significantly lower, and basal plasma cortisol was significantly higher, in the patients. In contrast, basal plasma ACTH determined by radioimmunoassay (RIA) was not significantly different between the two groups. The ACTH response to ovine corticotropin-releasing hormone (oCRH), whether measured specifically as ACTH1-39 or by the less-specific RIA, was highly significantly lower in the depressives than in the controls. However, neither the cortisol response to oCRH nor its response to low-dose ACTH 1-24 differed significantly between groups. In both groups of subjects, correlations between adrenal gland volume and all the hormone measures were low, and none represented more than 4% shared variance. In the patients, adrenal volume did not correlate significantly with duration of the present episode, lifetime number of episodes, melancholic subtype, Hamilton Depression Scale total score, or the Hamilton suicidality item. However, adrenal volume was significantly positively related to the somatization factor of the Hamilton scale, which was almost totally accounted for by the specific items of somatic symptoms and somatic anxiety.

Adolescent↗
PubMed1991

Testicular tumors in congenital adrenal hyperplasia: steroid measurements from adrenal and spermatic veins.

The present study reports the case of a 25-yr-old man with congenital adrenal hyperplasia due to 21-hydroxylase deficiency in whom bilateral testicular tumors did not regress after suppressive treatment with dexamethasone. Catheterization of left testicular and adrenal veins confirmed the enzyme deficiency in the gonadal lesions. The presence of specific 11 beta-hydroxylated steroids (11 beta-hydroxyandrostenedione, 21-deoxycortisol, and 21-deoxycorticosterone) in the gonadal vein demonstrated the adrenal nature of the testicular tumor. In addition, catheterization allowed further study of the secretion of mineralocorticoids and androgens in the adrenal venous effluent. Plasma levels of deoxycorticosterone were increased in the peripheral vein and decreased in the adrenal vein, confirming the conversion of progesterone by peripheral 21-hydroxylase activity. Plasma levels of delta 5-3 beta-hydroxysteroids, particularly dehydroepiandrosterone and its sulfate, were very low, suggesting a sustained stimulation of 3 beta-hydroxysteroid dehydrogenase activity. This study documents that in patients with congenital adrenal hyperplasia and bilateral testicular tumors, catheterization of a gonadal vein measuring specific 11 beta-hydroxylated steroids confirms the adrenal nature of the gonadal lesions.

Adrenal Cortex Hormones↗