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PubMed1988

The innervation of the adrenal gland. II. The source of spinal afferent nerve fibres to the guinea-pig adrenal gland.

The sensory innervation of the guinea-pig adrenal medulla was studied using the fluorescent retrograde tracer Fast Blue. Labelled neurons were found in the dorsal root ganglia at segments T3-L2, the greatest contribution arising from T10 representing 15.2% of the total number of labelled cells. Labelling was ipsilateral to the site of injection of tracer into the adrenal medulla and the labelled neurons ranged in size between 6 and 36 microns. The overall size distribution fell into two groups of between 6 and 15 microns and of between 18 and 36 microns. Presumed sensory nerve endings were found in the adrenal medulla associated with chromaffin cells and vascular elements. The nerve endings were ovoid to spherical and densely packed with mitochondria. It is concluded that events occurring in the guinea-pig adrenal medulla, and possibly cortex, are monitored by sensory nerve terminals whose cell bodies lie within dorsal root ganglia. The exact distribution of the sensory nerve terminals within the adrenal gland is yet to be determined.

Adrenal Glands↗
PubMed1985

Monoclonal antibodies against bovine adrenal cytochrome P-450(11 beta) and cytochrome P-450SCC. Their isolation, characterization and application to immunohistochemical analysis of adrenal cortex.

Seven monoclonal antibodies directed against bovine adrenocortical cytochrome P-45011 beta were isolated. They were found to be immunoglobulins each having distinct affinity to the antigen. Five clones had IgG1 heavy chains, whereas the other two had IgG2b heavy chains. All the clones had kappa light chains. All the monoclonal antibodies recognized a protein among mitochondrial proteins of bovine adrenal cortex, whose mol. wt, 50,000, was the same as that of cytochrome P-45011 beta. Among the monoclonal antibodies isolated, monoclonal antibody 258 recognized a protein of Mr 50,000 in rat adrenal mitochondria, a protein of Mr 47,000 in pig adrenocortical mitochondria, a protein of Mr 50,000 in guinea pig adrenal mitochondria, a protein of Mr 55,000 in rabbit adrenal mitochondria and a protein of Mr 50,000 in human adrenocortical mitochondria. These results suggest that each of these proteins, having a mol. wt around 50,000, recognized by monoclonal antibody 258 is very likely to be the cytochrome P-45011 beta of adrenocortical mitochondria of each animal species. Monoclonal antibody 42718 inhibited by 50% the steroid hydroxylation activity of cytochrome P-45011 beta. In addition to the monoclonal antibodies against cytochrome P-45011 beta, three monoclonal antibodies directed against bovine adrenocortical cytochrome P-450SCC were also isolated and characterized. Immunohistochemical staining of bovine adrenal cortex with the use of these two kinds of monoclonal antibodies revealed that the contents of both cytochrome P-45011 beta and cytochrome P-450SCC were greater in the zona fasciculata and zona reticularis than in the zona glomerulosa. Electron microscopical observation of immunoperoxidase-stained preparations confirmed the presence of these cytochromes in the mitochondria.

Adrenal Cortex↗
PubMed1997

Effects of pneumadin (PNM) on the adrenal glands. 6. Further studies on the inhibitory effect of PNM on dexamethasone-induced atrophy of the rat adrenal cortex.

Pneumadin (PNM) is a biologically active decapeptide, which has previously been found to enhanced rat adrenal growth; the mechanism is indirect and probably involves the stimulation of both arginine-vasopressin (AVP) and ACTH release. The effects of 2- and 6-day PNM administration on the atrophic adrenal cortices of rats treated for 8 and 12 days, respectively, with daily subcutaneous injections of 15 or 40 g/100 g body weight of dexamethasone (Dx) were investigated. Morphometry showed that PNM counteracted Dx-induced adrenal atrophy, by preventing the decrease in volume and number of the parenchymal cells. PNM raised aldosterone and corticosterone production of adrenal quarters from Dx-treated rats, but it did not evoke significant changes in the plasma concentrations of the two hormones. The preventive effect of PNM was only partial and almost exclusively evident in rats administered the lower dose of Dx. In light of these findings the following conclusions are drawn: (i) PNM is able to partially overcome the Dx-induced inhibition of the rat hypothalamo-pituitary-adrenal axis, probably by stimulating the pituitary release of AVP and ACTH, that in turn enhance adrenocortical growth; (ii) the PNM-induced improvement of the secretory capacity of atrophic adrenocortical cells is not sufficient to raise the blood level of corticosteroid hormones; and (iii) Dx exerts a direct inhibitory action on adrenocortical cells, which is not counteracted by PNM.

Adrenal Cortex↗
PubMed1976

Association of precipitating anti-adrenal anti-adrenal antibodies with moniliasis-polyendocrinopathy syndrome.

The association of precipitating anti-adrenal antibodies with different subgroups of idiopathic Addison's disease were studied. We had previously found these antibodies in patients with the moniliasis-polyendocrinopathy syndrome. Sera of 36 adult patients suffering from different froms of Addison's disease were examined for the presence of adrenal antibodies demonstrable either by immunofluorescence (IFL) or by gel diffusion. 3 of the 17 patients with tuberculous and 17 of 19 patients with idiopathic Addison's disease had IFL antibodies but only one had precipitating antibodies. There was one typical case of Schmidt's syndrome, and four additional cases with Addison's disease combined with diabetes or thyroiditis, who may later develop the syndrome. None of htese patients had precipitating anti-adrenal antibodies. The only patients with precipitating adrenal antibodies had the moniliasis-polyendocrinopathy syndrome. He was not typical as Addison' disease appeared unusually late and he did not have hypoparathyroidism. The presence of precipitating anti-adrenal antibodies in this patient, and the absence of these in other groups of Addison's disease, is further evidence for the association of precipitating antibodies with the moniliasis-polyendocrinopathy syndrome.

Addison Disease↗
PubMed1995

Expression of DAX-1, the gene responsible for X-linked adrenal hypoplasia congenita and hypogonadotropic hypogonadism, in the hypothalamic-pituitary-adrenal/gonadal axis.

DAX-1, an orphan member of the nuclear hormone receptor superfamily, is responsible for X-linked adrenal hypoplasia congenita (AHC) and the frequently associated hypogonadotropic hypogonadism (HH). The entire DAX-1 genomic region has been sequenced and a putative steroidogenic factor-1 response element has been identified in the promoter region of the gene. The purpose of these investigations was to determine if DAX-1 was expressed in the central nervous system, particularly the hypothalamus and pituitary, in order to better understand the relationship of mutations in this gene to HH associated with AHC. We used Northern blot analysis and reverse transcription PCR to demonstrate that DAX-1 was expressed in the hypothalamus and the pituitary, and to confirm its expression in adrenal cortex and gonads. The expression of DAX-1 in these tissues indicates the involvement of DAX-1 in the development of the reproductive system at multiple levels within the hypothalamic-pituitary-adrenal/gonadal axis. We also observed the expression of DAX-1 in a human adrenocortical carcinoma cell line, NCI-H295, that has features characteristic of the fetal adrenal cortex. Therefore, NCI-H295 cells will be a useful cellular model for investigating the involvement of DAX-1 in the regulation of steroidogenesis.

Adrenal Cortex↗
PubMed1975

Evidence for a plasma membrane calcium pump in bovine adrenal medulla but not adrenal cortex.

Continuous sucrose density gradient subfractions from bovine adrenal medullary microsomes were found to accumulate 45-Ca-2+ in the presence of ATP and ammonium oxalate mainly in subfractions of intermediate density. (Na-++K-+)-ATPase (plasma membrane marker) and Ca-2+-ATPase activities were also concentrated in these intermediate subfractions but thiamine pyrophosphatase (Golgi apparatus marker) was not. NADH oxidase (endoplasmic reticulum marker) activity was distributed throughout all subfractions. 45-Ca-2+ accumulation in adrenal cortical microsomes was found to rise and fall in parallel with thiamine pyrophosphatase but not with (Na-++K-+)-ATPase or NADH oxidase activities. Accumulation of 45-Ca-2+ in membrane vesicles in these experiments suggests the existence of a calcium transfer mechanism in plasma membranes of the adrenal medulla but not adrenal cortex.

Adenosine Triphosphatases↗
PubMed1998

Elevated post-dexamethasone suppression cortisol concentrations correlate with hormonal alterations of the hypothalamo-pituitary adrenal axis in patients with adrenal incidentalomas.

OBJECTIVE: It has recently been suggested that autonomous cortisol production may lead to subclinical glucocorticoid excess in a substantial number of patients with incidentally discovered adrenocortical adenomas. Following a standard low-dose dexamethasone suppression test (LDDST) cortisol concentrations are frequently incompletely suppressed in patients with adrenal incidentalomas, due to an ACTH-independent secretion of cortisol by the adrenal mass. Thus, post LDDST cortisol concentrations may provide a measure of the degree of autonomous glucocorticoid secretion, but hormonal alterations in relation to post-LDDST cortisol concentrations have not been thoroughly investigated. PATIENTS AND MEASUREMENTS: 61 patients with radiological features highly suggestive of adrenal adenomas were studied. These included 43 women, 18 men; mean age 59 +/- 1.4, range: 25-76 years; BMI 30.9 +/- 0.8 kg/m2 and waist:hip ratio 0.90 +/- 0.016. All subjects underwent a standard LDDST, as follows: after a 48-hr stabilisation period, 24-hr urine collections for basal urinary free cortisol (UFC) were performed. Basal serum cortisol and plasma ACTH were measured at 8 AM and at midnight the following day, and subjects started dexamethasone 0.5 mg 6 hourly for 2 days. Post-dexamethasone cortisol and ACTH levels were measured at 8 AM, 6-hrs after the last dose of dexamethasone. Blood samples for dehydroepiandrosterone sulphate (DHEAS) and serum lipids were obtained on the morning preceding dexamethasone administration. RESULTS: Post-LDDST cortisol concentrations correlated positively with the size of the adenoma (r = +0.527, P < 0.001). There was a negative rank correlation of post-LDDST cortisol concentrations and basal ACTH levels at 0900 h (rs = -0.426, P < 0.001) and DHEAS (rs = -0.380, P = 0.006). Moreover, there was a good rank correlation between DHEAS and basal ACTH levels (rs = +0.456, P < 0.001). A positive rank correlation was observed between post-LDDST cortisol concentrations and midnight cortisol concentrations (rs = +0.317, P = 0.020). As recent studies have suggested that post-LDDST cortisol levels higher than 70 nmol/l may indicate significant hypercortisolism comparisons were also performed between patients divided according to post-LDDST cortisol values into 3 groups: Group A, > 70 nmol/l (19 pts); Group B, 30-70 nmol/l (27 pts); Group C, < 30 nmol/l (15 pts). Although there was no difference in basal cortisol and UFC values between these groups, ACTH and DHEAS levels were significantly lower, and midnight cortisol significantly higher in group A compared to group C patients (P = 0.030, P = 0.017 and P = 0.001 respectively). Cholesterol and triglyceride levels were slightly albeit significantly higher in group A compared to group C patients (P < 0.05). CONCLUSIONS: It is concluded that higher post-low dose dexamethasone cortisol concentrations are associated with lower ACTH and dehydroepiandrosterone sulphate, higher midnight cortisol concentrations and larger adenomas. These findings are consistent with the hypothesis that post-low dose dexamethasone cortisol concentrations represent a useful index in assessing subtle glucocorticoid autonomy in patients with adrenal adenomas.

Adenoma↗
PubMed2006

[Giant bilateral adrenal myelolipoma associated with congenital adrenal hyperplasia].

BACKGROUND: Myelolipoma is a rare benign tumor formed by mature fat tissue with strata of haematopoiesis. It is mainly asymptomatic, only large myelolipomas manifest themselves by abdominal discomfort, bleeding or by symptoms of oppressing adjacent organs. It is usually localized in the region of the adrenal gland. Myelolipomas are mostly clinically inert, only a small number of them are associated with Cushing's type of endocrine disorders, Conn's syndrome, Addison's disease, etc. PATIENT AND METHODS: The authors present a rare case of a giant bilateral myelolipoma emerging out of the adrenal gland cortex in a congenital adrenal hyperplasia, with steroid 21-hydroxylase deficiency, in a woman with pronounced virilism. The principal diagnostic methods include sonography and computer tomography. The therapy available is either a surgical extirpation in the case of large or growing myelolipomas or observation in the case of small ones (< 5 cm). RESULTS: The condition was resolved by bilateral adrenalectomy with extirpation of both myelolipomas and subsequent hormonal substitution treatment during which there was a gradual regression of virilising symptoms. CONCLUSIONS: The coincidence of myelolipoma and congenital disorder with subsequent overproduction of the adrenocorticotropin hormone and androgens, might be explained by the incipient of myelolipoma through chronic hormonal stimulation of the adrenal gland cortex. However, the etiopathogenesis of myelolipoma is still unclear.

Adrenal Gland Neoplasms↗
PubMed1984

[Technic of real-time ultrasonic examination of the adrenal glands and adrenal gland tumors].

A prospective examination was carried out to determine the optimum technique for demonstrating the adrenal glands; there were 60 normal persons, 16 with small adrenal tumours (average size 13 mm.) and 10 with large adrenal tumours (average size 38 mm.). A normal adrenal gland was identified only once amongst the 60 patients as a hypoechoic structure. Fifteen of the 16 small, and eight of nine large tumours could be demonstrated sonographically. An intercostal approach was particularly suitable for showing the suprarenal region and for small tumours. Large tumours could be shown by a ventral, lateral or dorsal approach.

Adenoma↗
PubMed1982

The steroid response to controlled adrenal stimulation in congenital adrenal hyperplasia.

Adrenal steroidogenesis has been studied in vivo in eleven patients aged 13-68 years with 21-hydroxylase deficiency, in one patient with 11 beta-hydroxylase deficiency and in ten female control subjects. Serum levels of the delta 5 3 beta-hydroxysteroids, pregnenolone (Pe), 17 alpha-hydroxypregnenolone (17Pe), dehydroepiandrosterone (DHEA) and androstenediol (Adiol) and their delta 4 3-keto counterparts, progesterone (Po), 17 alpha-hydroxyprogesterone (17Po) androstenedione (Adione) and testosterone as well as of 11-deoxycortisol and cortisol were measured during acute adrenal suppression with dexamethasone followed by stimulation with synthetic 1-24 ACTH. In the seven patients with 21-hydroxylase deficiency who were on adequate glucocorticoid therapy, grossly exaggerated responses of 17Po and Po to ACTH were nevertheless preserved. In contrast, there was a grossly subnormal response of 17Pe, DHEA and Adiol to ACTH, and low basal levels of DHEA-sulphate. In the untreated patients the response of 17Pe and DHEA was normal. The Adione response was exaggerated in untreated and normal in treated cases. Similar findings obtained in the patient with 11 beta-hydroxylase deficiency who was studied after 6 weeks without replacement therapy. Our findings demonstrate that production of adrenal steroids that are associated with the adrenarche is not exaggerated in untreated CAH, and is grossly suppressed in treated cases. These findings are compatible with the hypothesis that intra-adrenal cortisol may initiate and/or maintain production of the delta 5 steroids by the zona reticularis that occurs in the human adrenarche.

Adolescent↗
PubMed1992

Investigation of adrenal function in women with oligomenorrhoea and hirsutism (clinical PCOS) from the north-east of England using an adrenal stimulation test.

OBJECTIVE: To determine the prevalence of adrenal enzyme dysfunction in women presenting with oligomenorrhoea and hirsutism, two clinical features of polycystic ovary syndrome (PCOS). DESIGN: A prospective study of women attending outpatient clinics with these complaints. Androstenedione, dehydroepiandrosterone (DHEA), 17-hydroxyprogesterone (17-OHP), 11-deoxycortisol and cortisol were measured before and after overnight dexamethasone suppression and at 60 minutes after adrenal stimulation by ACTH injection. SUBJECTS: Fifty women with clinical features of PCOS and 37 control women with regular cycles and normal hair distribution from the catchment area of the Royal Victoria Infirmary which includes Newcastle upon Tyne, Co. Durham, Cleveland, Cumbria and Northumberland. MEASUREMENTS: Number of women with steroid responses to ACTH beyond the normal range, as defined by the responses of the control group and in previous studies. RESULTS: Nineteen women (38%) were found to have some abnormality. One woman (2%) was identified with 21-hydroxylase (21-OHase) deficiency and a second (2%) had an increase in 17-OHP compatible with the heterozygote state for 21-OHase deficiency. Four women (8%) had isolated elevations in the DHEA response consistent with minimal 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) deficiency. Thirteen women (26%) showed increases in both androstenedione and DHEA, or androstenedione alone, compatible with enhanced 17-20 lyase activity. CONCLUSIONS: Twelve per cent of the group showed evidence consistent with an adrenal enzyme deficiency; 26% had results in keeping with increased adrenal androgen production without an enzyme deficiency. These findings may be of relevance both in the pathogenesis of the features of PCOS and in determining appropriate treatment for individual patients.

3-Hydroxysteroid Dehydrogenases↗
PubMed1990

Steroidogenic enzyme activities, morphology, and receptor studies of a testicular adrenal rest in a patient with congenital adrenal hyperplasia.

Steroid-secreting tumors of the testis have generally been considered to be of Leydig cell origin. Testicular tumors in patients with congenital adrenal hyperplasia have been thought to be adrenal rests, but no conclusive evidence supporting the hypothesis has been presented. We report a morphological and biochemical analysis of a patient with 21-hydroxylase deficiency who developed bilateral nodular hyperplasia of steroid-secreting tissue within the testis, despite suppression therapy with both exogenous glucocorticoids and testosterone. The tissue was formed of confluent nodules of homogenous cells. Electron microscopy showed the cells to have abundant smooth endoplasmic reticulum, well developed Golgi apparatus, and mitochondria with predominantly tubular cristae, features characteristic of steroid-secreting cells of adrenocortical origin. Crystals of Reinke were not observed. Functional studies in vivo showed a marked response to ACTH infusion, with 17-hydroxyprogesterone rising from 56 to 13,500 ng/mL, cortisol from less than 2 to 19 micrograms/dL, and testosterone from 369 to 629 ng/dL, with an attendant increase in testicular size and pain over 48 h. Receptor studies in vitro revealed no gonadotropin receptors, but abundant angiotensin-II receptors. Enzyme activity analysis in vitro showed undetectable 21-hydroxylase activity and an enzyme profile consistent with adrenocortical cells rather than Leydig cells. Based on these morphological and biochemical findings, we conclude that the nodular steroidogenic tissue that replaced this patient's testes was of adrenal origin. The study documents for the first time the development of adrenocortical tumors from adrenal rest tissue within the testis.

Adrenal Glands↗
PubMed1992

Pituitary-adrenal responses to corticotropin-releasing hormone in different degrees of adrenal 21-hydroxylase deficiency.

21-Hydroxylase congenital adrenal hyperplasia (21-OHCAH) involves a primary defect of the adrenal gland and a secondary involvement of ACTH secretion. The responses of the pituitary-adrenal axis to ovine CRH (oCRH, 1 micrograms/kg) were examined in subjects with different degrees of 21-OH deficiency. We studied 43 subjects: 7 classical and 6 nonclassical (NC) 21-OHCAH patients, 15 heterozygotes (HT) and 15 control subjects. Baseline plasma ACTH levels were higher in classical CAH than in NC-CAH, HT, and control subjects (mean +/- SEM, 66 +/- 14, 6 +/- 1.6, 4 +/- 0.5, and 5 +/- 0.5 pmol/L, respectively). The mean plasma ACTH response to oCRH in NC-CAH (17 +/- 3 pmol/L) was higher than in controls and HT (9 +/- 0.8 and 11 +/- 1.5 pmol/L). The highest ACTH responses to oCRH were obtained for classical CAH patients (126 +/- 29 pmol/L). Plasma cortisol rose after oCRH in control, HT, and NC-CAH patients but did not change in classical CAH. After oCRH, plasma 17-hydroxyprogesterone (17-OHP) were 4 +/- 0.5, 8 +/- 1.6, 93 +/- 28, and 359 +/- 110 nmol/L for controls, HT, NC-CAH, and classical patients, respectively. There was a significant correlation (r = 0.70) between 17-OHP and the ACTH responses to oCRH. The 17-OHP responses to oCRH were also correlated (r = 0.94) with the 17-OHP responses to the synthetic ACTH test. We conclude that the release of endogenous ACTH by oCRH result in graded 17-OHP responses on 21-OH deficiency. The present study also suggests that different degrees of adrenal biosynthetic defect may result in graded ACTH responses to oCRH.

17-alpha-Hydroxyprogesterone↗
PubMed1976

[Extra-adrenal pheochromocytoma associated with bilateral diffuse-nodular hyperplasia of the adrenal cortex and micro-macrofollicular goiter].

At autopsy there was found extra-adrenal pheochromocytoma, bilateral diffuse-nodulous and adenomatous hyperplasia of the adrenal cortex in a female patient who had suffered for a long time from high arterial pressure. In the enlarged thyroid gland there was revealed micro-macrofollicular colloid goiter with basedowification. The morphological changes and results of an investigation of the liquor (drop in the content of potassium) justify the assumption that in this case there is a combination of extra-adrenal pheochromocytoma with hormonally active rearrangement of the adrenal cortex--primary hyperaldosteronism and basedowified goiter.

Adrenal Cortex↗
PubMed2002

Adrenal gland hypofunction in active polymyalgia rheumatica. effect of glucocorticoid treatment on adrenal hormones and interleukin 6.

OBJECTIVE: To evaluate hypothalamic-pituitary-adrenal (HPA) axis function in patients with recent onset polymyalgia rheumatica (PMR) not previously treated with glucocorticoids; and to detect possible correlations between adrenal hormone levels, interleukin 6 (IL-6), and other acute phase reactants at baseline and during 12 months of glucocorticoid treatment. METHODS: Forty-one PMR patients of both sexes with recent onset disease and healthy sex and age matched controls were enrolled into a longitudinal study. Patients were monitored for serum cortisol, dehydroepiandrosterone sulfate (DHEAS), androstenedione (ASD), and clinical and laboratory measures of disease activity such as C-reactive protein and IL-6 concentrations at baseline and after 1, 3, 6, 9 and 12 months of glucocorticoid treatment. To assess dynamic HPA axis function, serum cortisol and plasma adrenocorticotropic hormone (ACTH) levels were evaluated in another 8 patients with recent onset PMR not treated with glucocorticoid in comparison to controls after challenge with ovine corticotropin releasing hormone (oCRH) test. In addition, serum cortisol and 17-hydroxyprogesterone (17-OHP) levels were evaluated after stimulation with low dose (1 microg) intravenous ACTH. RESULTS: Serum cortisol and ASD levels of all PMR patients at baseline did not differ from controls. During followup, cortisol levels dipped at one and 3 months. Serum DHEAS levels in all patients were significantly lower than in controls at baseline. In female PMR patients a significant correlation was found at baseline between cortisol levels and duration of disease. Serum concentrations of IL-6 at baseline were significantly higher in PMR patients than in controls. During 12 months of glucocorticoid treatment IL-6 levels dropped significantly at one month; thereafter they remained stable and did not increase again despite tapering of the glucocorticoid dose. After oCRH stimulation, a similar cortisol response was found in patients and controls. After ACTH administration, a significant cortisol peak was detected in patients and controls, whereas no significant difference in cortisol area-under-the-curve (AUC) was found between the groups. In contrast, ACTH induced a significantly higher (p < 0.05) peak of 17-OHP and AUC in PMR patients than in controls. CONCLUSION: This study found reduced production of adrenal hormones (cortisol, DHEAS) at baseline in patients with active and untreated PMR. The defect seems mainly related to altered adrenal responsiveness to the ACTH stimulation (i.e., increased 17-OHP), at least in untreated patients. The 12 month glucocorticoid treatment of patients reduced the production of inflammatory mediators (i.e., IL-6) in a stable manner that persisted after glucocorticoids were tapered.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

Effects of combined hypophysectomy and cyproterone acetate on the adrenal chromaffin cells of the rat. Evidence for postnatal migration of adrenal chromaffin cells.

A light and electron-microscopic study was performed concerning the effects of hypophysectomy (HP) followed by cyproterone acetate (CA) treatment on the adrenal chromaffin cells of the rat. The latter drug is reported to interfere with steroid biosynthesis. When given following HP, CA was found to induce degeneration in the inner cells of the zona fasciculata and a marked fall in the blood corticosterone level. The adrenal chromaffin cells which were depleted after the administration of reserpine at the beginning of the experiment failed to recover two weeks later. In addition, some of the depleted chromaffin cells migrated towards the outer cells of the zona fasciculata, had the appearance of pheochromoblasts and showed features of increased synthetic activity. The results are discussed in the light of the generally accepted functional relationship between the cells of the adrenal cortex and the medulla and following a marked fall in the concentration of blood corticosterone, a chemobiotaxis is suggested between the chromaffin and adrenal cortical cells.

Adrenal Cortex↗
PubMed1984

[The coexistence of neuropeptides and catecholamines in the adrenal gland. Research on paracrine effects on adrenal cortex cells].

The aim of the present review was to compare in mammals and amphibians the data concerning the presence of neuropeptides in the chromaffin cells and the possible action of these substances on adrenocortical cell function. Major homologies are to be found concerning the coexistence in chromaffin granules of catecholamines, Met-and Leu-enkephalins, and their precursor, proenkephalin A. However, the inhibitory action that might be exerted by enkephalins in vitro on corticosteroid production in mammalian adrenal gland, does not occur in amphibia. Dynorphin has been isolated in bovine adrenal medulla extracts; the presence of this opioid peptide has not been reported yet in amphibian interrenal tissue. All chromaffin cells of the frog interrenal gland contain VIP-like immunoreactivity whereas this neuropeptide is not contained in the adrenal medulla of mammals, exept in certain pheochromocytomas. In the frog, VIP, Metenkephalin and catecholamines are co-sequestered in the same chromaffin granules. In addition, synthetic porcine or chicken VIP stimulate in vitro the secretion of corticosteroids by frog interrenal fragments. In mammals, the steroidogenic action of VIP has been observed exclusively in tumor cell lines. The existence of somatostatin has been demonstrated in the human adrenal medulla and in pheochromocytomas, but not in amphibia. Somatostatin has been found to inhibit the response of adrenocortical cells to angiotensin II in mammals. A similar effect of somatostatin was not observed in amphibia. The coexistence of VIP and catecholamines in frog chromaffin granules and the stimulatory effect exerted by VIP on corticosteroidogenesis suggest that, in these animals, VIP may be co-liberated with noradrenaline during stress conditions, and thus may act locally on adrenocortical cells to stimulate corticosteroid secretion.

Adrenal Cortex↗
PubMed1968

Quantitative estimation of 17alpha-hydroxypregn-4-ene-3,20-dione (17alphaOH-progesterone) in adrenal venous blood and adrenal glands.

1. A method is described for the accurate estimation of small quantities of 17alpha-hydroxypregn-4-ene-3,20-dione (17alphaOH-progesterone) in blood and adrenal glands.2. The dog adrenal was found to secrete 17alphaOH-progesterone under conditions of operative stress at a rate of 5-10 mug/g tissue/hr. This is similar to the secretion rate of aldosterone.3. The secretion of 17alphaOH-progesterone was decreased after hypophysectomy and increased in response to adrenocorticotrophic hormone (ACTH).4. The adrenal gland of the dog, the monkey and the guinea-pig was found to contain between 0.6 and 6 mug of 17alphaOH-progesterone/g tissue. The concentration was usually somewhat smaller than that of pregnenolone or progesterone and between 1 and 20% of the concentrations of the glucocorticoids.5. A comparison of adrenal steroid contents and secretion rates under conditions of stress indicates a rate of synthesis in the order of 30-40 n-moles of 17alphaOH-progesterone/g adrenal tissue/min.

Journal Article↗