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PubMed1992

New developments in the pathologic diagnosis of adrenal cortical neoplasms. A review.

In the past decade, our knowledge of neoplasms arising in the adrenal cortex has been expanded greatly. Histologic criteria for distinguishing benign from malignant adrenal cortical neoplasms have been developed. In this review, three systems useful in making this distinction are reviewed and compared. Pathologic indicators of prognosis for adrenal cortical carcinomas have been proposed and these include mitotic rate, stage, surgical resectability, nuclear grade, and tumor size. Of these, mitotic rate appears to be the best indicator. Adrenal cortical carcinomas with a high mitotic rate behave most aggressively. The role of immunohistochemical and DNA content analysis in the diagnosis of adrenal cortical neoplasms is limited. Neoplastic adrenal cortical cells contain a low density of keratins that is often destroyed by routine fixation and paraffin embedding. Thus, the absence of keratins in adrenal cortical neoplasms, particularly carcinomas, in routinely processed tissue should not dissuade the pathologist from making the diagnosis of an epithelial neoplasm. DNA content analysis has revealed an imperfect correlation between DNA ploidy and histologic diagnosis. Some adrenal cortical adenomas contain aneuploid stem cell lines, whereas some adrenal cortical carcinomas have diploid DNA content. Molecular genetic analyses suggest that one or more tumor suppressor genes may be involved in the pathogenesis of adrenal cortical neoplasms.

Adrenal Cortex Neoplasms↗

PubMed1998

Weight of adrenal glands may be increased in persons who commit suicide.

In a previous study, increased weight of the adrenal glands was found in a small group of persons who committed violent suicides. This finding was confirmed in our study, which comprised a group of 42 suicide cases and 37 control cases. Further analysis with special consideration toward a "relative adrenal weight" (weight/body surface) revealed that a relative combined adrenal weight >6 g/m2 may be a morphologic sign of a depressive disorder prior to death if no other disease with a known effect on the adrenals is present. These results are consistent with clinical computed tomographic findings of enlarged adrenals in depressed patients. In all suicide cases the police records were reviewed and a postmortem psychiatric diagnosis conducted to investigate whether a correlation between adrenal weight and the "severity" of depression or type of psychiatric disorder exists. In thirteen cases, psychiatric treatment prior to death was known, and a postmortem severity score of depressive disease was formed. No influence of this score or the postmortem diagnosis on the adrenal weight, however, could be detected. Also, the increase in weight of adrenal glands could not be explained by a suspected or proven preceding drug therapy or use. The effect on the pituitary-adrenal-axis by depressive disorders and changes in serotonin metabolism have been investigated repeatedly; mainly reported are increased levels of corticotropin-releasing hormone (CRH) and adrenocorticotropic hormone (ACTH) in the depressive interval, which may lead to a growth of the adrenal glands.

Adrenal Glands↗

PubMed2003

Feasibility of laparoscopic adrenalectomy for large adrenal masses.

Laparoscopic adrenalectomy (LA) is a preferred method for the removal of small adrenal masses. However, the role of LA for surgical treatment of large adrenal masses is less established. We evaluated the outcomes of LA for large (>/=5 cm) adrenal masses. We retrospectively reviewed 24 consecutive patients who underwent LA for large adrenal masses at a tertiary care university hospital. The average age of the 24 patients was 49 years, and each underwent laparoscopic resection of a large adrenal mass. All LAs were performed via a lateral transperitoneal approach. The average (+/- standard deviation) size of the masses was 6.8 +/- 1.5 cm (range, 5-11). Pathologic diagnoses included adrenal cortical adenoma (10 cases), pheochromocytoma ( 7), cyst/pseudocyst ( 3), myolipoma ( 2), and adrenal cortical hyperplasia ( 2). Statistical analysis was performed with a two-sample t test. The average operating time was 178 +/- 55 minutes (range, 120-300), and average blood loss was 87 +/- 69 mL (range, 20-300); the averages were nonsignificantly greater in the right LA group than in the left LA group (203 vs. 166 minutes, P = 0.89; 124 vs. 77 mL, P = 0.14). The average duration of nothing-by-mouth (NPO) status was 0.7 days (range, 0-4), and the average time until return to a regular diet was 1.74 +/- 0.9 days (range, 1-5). The average length of stay was 2.5 +/- 1.9 days (range, 1-10). One patient had a transient episode of pseudomembranous colitis. There were no conversions to open adrenalectomy and no major morbidities or mortalities. LA is safe and effective for surgical treatment of large adrenal masses. Both right and left large adrenal masses can be approached laparoscopically with equal success. The role of minimally invasive approaches to adrenal malignancies necessitates further investigation.

Adrenal Gland Neoplasms↗

PubMed1993

Activation of magnocellular vasopressin responses to non-osmotic stress after chronic adrenal demedullation in rats.

Increases in plasma VP in response to osmotic stimulation are critical for water conservation, while VP released into the pituitary portal circulation is an important regulator of ACTH secretion and does not contribute to plasma VP levels. The role of the adrenal medulla in the specificity of these responses was studied in rats subjected to osmotic and non-osmotic stress two months following adrenal demedullation or sham operation. Basal and stimulated plasma corticosterone, aldosterone, ACTH and PRA levels in adrenal demedullated rats were similar to those in the sham operated groups indicating recovery of adrenocortical function. Basal plasma VP level were similar in sham operated controls and adrenal demedullated rats (0.93 +/- 0.13 and 1.0 +/- 0.1 pg/ml, respectively) and rose to comparable levels in both groups following 48 h osmotic stimulation by water deprivation (14.4 +/- 1.3 and 20.7 +/- 3.4, respectively). On the other hand, while in sham operated rats, immobilization for 15 min, a non-osmotic stress, had no effect on plasma VP levels in control or water deprived (2.0 +/- 0.9 and 15.0 +/- 2.7 pg/ml), in adrenal demedullated rats, caused dramatic increases in plasma VP from 1.0+/-0.1 to 126.0+/029.9 pg/ml in controls, and from 20.7 +/- 3.4 to 155 +/- 37 pg/ml in water deprived rats. Intraperitoneal hypertonic saline injection, a combination of osmotic and painful stress, caused much higher increases in plasma VP in adrenal demedullated rats (138.0 +/- 22.1 compared with 34.7 +/- 3.7 pg/ml in sham operated rats). Water deprivation potentiated this response to 70.0 +/- 8.3 and 295 +/- 24 pg/ml in sham operated and adrenal demedullated rats, respectively. VP mRNA measured by in situ hybridization, and irVP measured by immunohistochemistry, were elevated in magnocellular neurones in the hypothalamus of adrenal demedullated rats. The demonstration of marked plasma VP responses to non-osmotic stimuli in adrenal demedullated rats, suggests a modulatory role for the adrenal medulla in the specificity of the secretory responses of the magnocellular and parvicellular vasopressinergic systems.

Adrenal Medulla↗

PubMed1990

Effects of nitrofurans on adrenal cortical tissue in chickens.

In chicken adrenal glands, aspartate transaminase (AST) activity is concentrated in the adrenal cortical cells. Administration of a bolus dose of furazolidone (200 mg/kg) to the birds produced a decrease in AST activity in the adrenal glands and a general disorganization in the ultrastructure of the adrenal cortical cells. Many adrenal cortical mitochondria appeared to be moribund, being swollen, without cristae or apparently empty. These effects preceded atrophy of the adrenal cortical tissue, which was most marked in the central part of the adrenal glands. The atrophy was still present after 12 weeks, and it is therefore suggested that nitrofurans may be useful in the treatment of Cushing's disease in other animal species. When furazolidone or furaltadone was given in the diet at therapeutic levels, blebs of an electron-dense substance developed in adrenal cortical mitochondria and AST activity in the adrenal glands was reduced. These effects were found to be reversible, and the treatments did not produce atrophy of the adrenal cortical tissue.

Adrenal Cortex↗

PubMed2000

Nociceptive neuroendocrine negative feedback control of neurogenic inflammation activated by capsaicin in the rat paw: role of the adrenal medulla.

Recently we have found that inhibition of bradykinin-induced synovial plasma extravasation by transcutaneous electrical stimulation at strengths which excite unmyelinated afferent axons is mediated by the hypothalamo-pituitary-adrenal axis. Here we tested whether stimulation of nociceptors in the rat paw by intradermally injected capsaicin inhibits bradykinin-induced synovial plasma extravasation and whether this inhibition is mediated by the hypothalamo-pituitary-adrenal or sympatho-adrenal axis. Furthermore, we tested whether inhibition of bradykinin-induced plasma extravasation generated by intraperitoneally injected capsaicin, which preferentially excites visceral afferents, is mediated by the hypothalamo-pituitary-adrenal or sympatho-adrenal axis. We used normal rats, subdiaphragmatically vagotomized rats, rats with denervated adrenal medullae and rats with acutely transected spinal cords at the segmental levels T1/T2 or T12/L1. Injection of capsaicin into the plantar or palmar surface of the paws produced a depression of bradykinin-induced plasma extravasation. The inhibition elicited from the forepaw was larger than that from the hindpaw. The inhibition of bradykinin-induced plasma extravasation elicited from both paws was potentiated by subdiaphragmatic vagotomy. Denervation of the adrenal medullae abolished the inhibitory effect of intradermal capsaicin in vagus-intact and in vagotomized animals. After spinalization at the segmental level T1/T2, capsaicin injected into the forepaw did not depress bradykinin-induced plasma extravasation either in vagus-intact or in vagotomized animals. Capsaicin injected into the hindpaw in these spinalized animals produced a small depression. After spinalization at the segmental level T12/L1 no depression was produced by capsaicin injected into the hindpaw. Depression of bradykinin-induced plasma extravasation generated by intraperitoneal injection of capsaicin in vagus-intact and in vagotomized animals was also abolished or attenuated after denervation of the adrenal medullae. This shows that this depression was also largely dependent on the activation of the sympatho-adrenal system. We conclude that depression of bradykinin-induced plasma extravasation during stimulation of nociceptors by capsaicin is mediated predominantly by the sympathoadrenal pathway. This finding differs from the inhibitory mechanism of depression of bradykinin-induced plasma extravasation generated by cutaneous electrical stimulation, which is mediated by the hypothalamo-pituitary-adrenal axis.

Adrenal Medulla↗

PubMed1991

Activation of tyrosine hydroxylase by nicotine in rat adrenal gland.

The administration of nicotine activates tyrosine hydroxylase in the rat adrenal gland. This activation is apparently maximal 25 min after a single subcutaneous injection of nicotine at 2.3 mg/kg. Repeated injections of nicotine (seven injections once every 30 min) are associated with a persistent activation of adrenal tyrosine hydroxylase for at least 3 h. The nicotinic receptor antagonist hexamethonium does not significantly inhibit the nicotine-mediated activation of tyrosine hydroxylase in innervated adrenal glands. However, hexamethonium completely blocks the activation of adrenal tyrosine hydroxylase by nicotine in denervated adrenal glands. Furthermore, even though a single injection of nicotine activates tyrosine hydroxylase in both innervated and denervated adrenal glands, repeated injections of nicotine do not activate tyrosine hydroxylase in denervated adrenal glands. Our results suggest that the systemic administration of nicotine activates adrenal tyrosine hydroxylase by two mechanisms: (1) via direct interaction with adrenal chromaffin cell nicotinic receptors; and (2) via stimulation of the CNS leading to the release from the splanchnic nerve of substances that interact with adrenal chromaffin cell receptors other than the nicotinic receptor.

Adrenal Glands↗

PubMed1986

Co-release of neuropeptide Y and catecholamines upon adrenal activation in the cat.

The release of neuropeptide Y (NPY)-like immunoreactivity (-LI) in relation to catecholamines from the cat adrenal was studied in anaesthetized animals. Abdominal surgery increased plasma levels of NPY-LI from 65 +/- 6 to 149 +/- 26 pmol l-1. A positive veno-arterial concentration gradient over the adrenal gland was found for both NPY-LI, adrenaline (Adr) and noradrenaline (NA) during basal conditions. Asphyxia for 2 min increased the output of both NPY-LI and catecholamines from the adrenal. Electrical stimulation of the splanchnic nerve caused a marked increase in adrenal output of NPY-LI and catecholamines. The adrenal content of NPY-LI, as well as the release of NPY-LI from the adrenal, was at least 1000-fold lower on a molar basis than that of catecholamines. The concentration of NPY-LI in the adrenal vein upon splanchnic nerve stimulation was in the nM range. Reversed-phase HPLC characterization revealed that NPY-LI in the adrenal, and in the adrenal venous plasma collected during splanchnic nerve stimulation, was closely related to synthetic porcine NPY. Stimulation with bursts of 20 Hz for 1 S with 10 s intervals for 2 min caused a four-fold higher output of NPY-LI and Adr compared to a continuous stimulation with 2 Hz, giving the same number of impulses. The NA output, however, was only slightly increased by burst stimulation. Guanethidine did not reduce the adrenal output of NPY-LI or catecholamines induced by splanchnic nerve stimulation, while the release was abolished by chlorisondamine.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

PubMed1981

Facilitation of secretion of catecholamines from rat and guinea-pig adrenal glands in potassium-free medium or after ouabain.

1. The effect of K deprivation on catecholamine (CA) secretion induced by transmural stimulation of the isolated perfused adrenal glands of the rat was studied. 2. In the absence of external K, secretion of CA evoked by transmural stimulation was greatly (2- to 7-fold) facilitated. The facilitation was inversely related to the frequency of stimulation. The duration of CA secretion upon stimulation was prolonged significantly in K-free medium as compared to that in Krebs solution. 3. CA secretion evoked by acetylcholine (ACh) in K-free Krebs solution was increased by about 40%, with little change in the duration of secretion. 4. Chronic denervation of the adrenal gland practically abolished secretory response induced by transmural stimulation without affecting secretion of CA by ACh. Perfusion of the denervated adrenal gland with K-free solution enhanced ACh-induced CA secretion by about 40%, and a secretory response to transmural stimulation became evident. 5. Spontaneous secretion of CA was increased from a control value of about 2 ng/min to 56 ng/min 35 min after perfusion with K-free Krebs solution. During enhanced spontaneous secretion, electrical stimulation of the adrenal gland produced facilitation of secretion. 6. Spontaneous secretion of CA in K-free medium was only slightly reduced by lowering Ca to 0.25 mM, but that evoked by stimulation was markedly depressed. However, spontaneous and evoked secretion in K-free medium were totally blocked upon removal of Ca and addition of 5 mM-EGTA. 7. Re-introduction of 2.5 mM-Ca 6 min after stimulation of the adrenal gland in 0.25 mM-Ca, K-free solution produced a marked secretory response. 8. Lowering of Ca to 0.25 mM immediately after stimulation of the adrenal gland in K-free solution significantly reduced the amounts of CA secreted in the post-stimulation period. 9. Ouabain (0.14-1.4 mM) did not enhance secretion of CA in unstimulated preparations or after transmural stimulation of the rat adrenal gland. ACh-induced secretion was more than doubled by ouabain. 10. Not only was spontaneous secretion of CA from the guinea-pig adrenal gland enhanced by K deprivation or ouabain, but secretion evoked by transmural stimulation or by ACh was also facilitated in K-free medium by ouabain (0.7-7.0 microM). 11. Enhanced secretion of CA in unstimulated preparations or after transmural stimulation of the adrenal gland, in the absence of K, has been attributed to the excess release of ACh from splanchnic nerve terminals. The enhanced release of ACh has been attributed to the elevation of free cellular CA resulting from blockade of the Na pump. On the other hand, ouabain facilitates CA secretin in the rat and guinea-pig adrenal glands predominantly by its effect on the chromaffin cells.

Acetylcholine↗

PubMed1987

Sensory fibres modulate histamine-induced catecholamine secretion from the rat adrenal medulla and sympathetic nerves.

1. We have studied the mechanism of catecholamine secretion induced by histamine from the adrenal medulla and sympathetic noradrenergic neurones in the rat, and the role of capsaicin-sensitive sensory nerves in this secretion. 2. Histamine at a dose of 1 mg/kg induced adrenaline and noradrenaline secretion by a non-neurogenic mechanism. In contrast, at a dose of 3 mg/kg it induced adrenaline and noradrenaline secretion by both non-neurogenic and neurogenic mechanisms. 3. The adrenaline released in response to histamine at 3 mg/kg was exclusively of adrenal origin whereas the noradrenaline released was of non-adrenal origin (most probably noradrenergic sympathetic nerves). As with its action on the adrenal, histamine induced noradrenaline secretion from these extra-adrenal tissues by both neurogenic and non-neurogenic mechanisms. 4. When adrenaline secretion from the adrenal gland was impaired by adrenal denervation and/or adrenalectomy, the plasma noradrenaline secretion was increased. This is most probably due to compensation from the rest of the sympathetic nervous system. This compensatory increase in noradrenaline was abolished by hexamethonium, which indicates that it was mediated by a cholinergic mechanism. 5. Pre-treatment of rats as neonates subcutaneously with capsaicin (a selective neurotoxin for certain sensory nerves) at a dose of 50 mg/kg, had no effect on the non-neurogenic secretion of catecholamine induced by histamine. In contrast, capsaicin pre-treatment abolished the neurogenic catecholamine secretion in response to histamine as well as the neurogenic compensatory increase in plasma noradrenaline levels that occurred when adrenaline secretion by the adrenal gland was impaired. 6. In the present study, by using histamine as a form of stress, we have been able to provide evidence not only (a) to confirm a role for capsaicin-sensitive sensory fibres in modulating neurogenic adrenaline secretion from the adrenal gland, but also (b) to suggest a similar role for these fibres in modulating neurogenic noradrenaline release from sympathetic noradrenergic nerves in response to histamine and in response to impairment of adrenaline secretion by the adrenal gland.

Adrenal Medulla↗

PubMedDate not supplied

Imaging of nontraumatic hemorrhage of the adrenal gland.

Nontraumatic hemorrhage of the adrenal gland is uncommon. The causes of such hemorrhage can be classified into five categories: (a) stress, (b) hemorrhagic diathesis or coagulopathy, (c) neonatal stress, (d) underlying adrenal tumors, and (e) idiopathic disease. Computed tomography (CT), ultrasonography (US), and magnetic resonance (MR) imaging play an important role in diagnosis and management. CT is the modality of choice for evaluation of adrenal hemorrhage in a patient with a history of stress or a hemorrhagic diathesis or coagulopathy (anticoagulant therapy). CT may yield the first clue to the diagnosis of adrenal insufficiency secondary to bilateral massive adrenal hemorrhage; such insufficiency is rare but life threatening. US is the modality of choice for evaluation of neonatal hematoma, and MR imaging is helpful for further characterization. MR imaging is also useful in the diagnosis of coexistent renal vein thrombosis. When an adrenal abscess is suspected, percutaneous aspiration and drainage under imaging guidance should be performed. Hemorrhage into an adrenal cyst or tumor can cause acute onset of symptoms and signs in a patient without discernible risk factors for adrenal hemorrhage. A hemorrhagic adrenal tumor should be suspected when CT or MR imaging reveals a hemorrhagic adrenal mass of heterogeneous attenuation or signal intensity that demonstrates enhancement.

Adrenal Gland Diseases↗

PubMed2004

Zone-specific cell proliferation during compensatory adrenal growth in rats.

Compensatory adrenal growth after unilateral adrenalectomy (ULA) leads to adrenocortical hyperplasia. Because zonal growth contributions are not clear, we characterized the phenotype of cortical cells that proliferate using immunofluorescence histochemistry and zone-specific cell counting. Rats underwent ULA, sham adrenalectomy (sham), or no surgery and were killed at 2 or 5 days. Adrenals were weighed and sections immunostained for Ki67 (proliferation), cytochrome P-450 aldosterone synthase (P450aldo, glomerulosa), and cytochrome P-450 11beta-hydroxylase (P45011beta, fasciculata). Unbiased stereology was used to count proliferating glomerulosa and fasciculata cells. Adrenal weight increased after ULA compared with sham and no surgery at both time points, and there was no difference between sham and no surgery. However, either ULA or sham increased Ki67-positive cells in the outer fasciculata at both time points compared with no surgery. Outer fasciculata-restricted proliferation is thus associated with adrenal weight gain in ULA but not sham. Experiment repetition using proliferating cell nuclear antigen and bromodeoxyuridine showed similar results. After ULA, adrenal DNA, RNA, and protein increased at both time points, whereas after sham, only adrenal DNA increased at 2 days. Compensatory growth thus results from hyperplasia and hypertrophy, whereas sham induces only a transient adrenal hyperplasia. Dexamethasone pretreatment prevented the increase in adrenal weight after ULA and blocked Ki67 labeling in the outer fasciculata but not zona glomerulosa in all groups. These results clearly show that the outer fasciculata is the primary adrenal zone responsible for compensatory growth, responding to steroid-suppressible stress signals that alone are ineffective in increasing adrenal mass.

Adrenal Glands↗

PubMed1981

Regulation of adrenal blood flow: response to hemorrhagic hypotension.

Adrenal blood flow was measured during hemorrhagic hypotension in pentobarbital-anesthetized dogs using the radioactive-microsphere technique. A decrease in adrenal vascular resistance occurred during hemorrhage that was sufficient to maintain adrenal blood flow at prehemorrhage levels even with a decrease in mean arterial blood pressure (MABP) to as low as 50 mmHG. Blockade of alpha- and beta-adrenergic receptors, H1- and H2-histamine receptors, and prostaglandin synthesis all decreased resting adrenal blood flow. However, blood flow did not decrease further with hemorrhage subsequent to these interventions. Neither cholinergic blockade (muscarinic) alone nor ganglionic blockade subsequent to cholinergic blockade changed adrenal blood flow. However, ganglionic blockade alone increased adrenal blood flow. Hemorrhage subsequent to hypophysectomy also did not change blood flow to the adrenal. These data suggest that the maintenance of adrenal blood flow during hemorrhagic hypotension to 50 mmHg MABP is independent of the autonomic nervous system, prostaglandin synthesis, histamine receptors, or an intact pituitary-adrenal axis, even though all of these systems do influence adrenal blood flow.

Adrenal Glands↗

PubMed1986

Suppression of adrenal renin in Dahl salt-sensitive rats.

We previously showed that adrenal renin is highest in the rat zona glomerulosa (ZG) and that low sodium or high potassium and nephrectomy increase adrenal ZG renin and aldosterone. Dahl salt-sensitive rats (S) have been shown to have lower plasma renin activity and plasma aldosterone and higher plasma 18-hydroxy-11-deoxycorticosterone than Dahl salt-resistant rats (R). In this study we assess the possible role of adrenal ZG renin in the suppression of aldosterone in S rats. Adrenal ZG renin was significantly decreased in S as compared with R rats even at 6 weeks of age, when both S and R rats are still normotensive (S = 7.2 +/- 0.2, R = 18.0 +/- 1.6 ng angiotensin I/mg protein/hr). Adrenal ZG aldosterone was also significantly lower in S than in R rats (S = 21.1 +/- 4.3, R = 39.5 +/- 3.6 ng/mg protein). Furthermore, the rise in adrenal ZG renin and aldosterone after nephrectomy in S rats was significantly less than that in R rats. To determine if the suppressed adrenal ZG renin of S rats is due to volume expansion, we studied the effect of a sodium-deficient diet on adrenal ZG renin in S and R rats. After 2 weeks of a sodium-deficient diet S rats had significantly lower basal adrenal ZG renin than did R rats (S = 7.6 +/- 0.4, R = 21.7 +/- 1.9 ng angiotensin I/mg protein/hr) and a marked blunting of the adrenal ZG renin response to nephrectomy (S = 13.6 +/- 1.1, DR = 167 +/- 16.1 ng angiotensin I/mg protein/hr).(ABSTRACT TRUNCATED AT 250 WORDS)

18-Hydroxydesoxycorticosterone↗

PubMed1985

A role for the adrenal renin-angiotensin system in the regulation of potassium-stimulated aldosterone production.

Potassium is a major regulator of aldosterone production. It also increases adrenal renin. The causal relationship between potassium and adrenal renin is not known. To evaluate the role of the intraadrenal renin-angiotensin (ANG) system in potassium-stimulated aldosterone synthesis and release, specific adrenal renin activity, PRA, and plasma aldosterone were measured during potassium loading or captopril treatment in the rat. Adrenal ANGs were determined using a HPLC system combined with RIA to obtain quantitative information on the components of the adrenal renin-ANG system. In addition, the effect of pretreatment with captopril on aldosterone production by isolated adrenal glomerulosa cells was examined. In intact animals potassium loading markedly increased adrenal renin and plasma aldosterone, whereas PRA was suppressed. The administration of captopril to rats in normal potassium balance did not suppress plasma aldosterone. Captopril treatment during potassium loading inhibited the potassium-induced increase in aldosterone. Furthermore, pretreatment with captopril suppressed adrenal ANG II and reduced the response of aldosterone production to extracellular potassium concentration by isolated adrenal glomerulosa cells in vitro. These results suggest that the adrenal renin-ANG system plays a significant role in the control of aldosterone production under potassium stimulation.

Adrenal Glands↗

PubMed1975

The mechanism of ACTH stimulation of adrenal ornithine decarboxylase activity.

The mechanism of action of adrenocorticotrophin (ACTH) stimulation of rat adrenal orticotrophin (ACTH) stimulation of rat adrenal ornithine decarboxylase activity was investigated. ACTH induction or ornithine decarboxylase activity was not prevented by administration of drugs that inhibit adrenal steroid biosynthesis. A dose of ACTH that produced maximal levels of adrenal cyclic AMP did not induce ornthine decarboxylase activity. Ovine growth hormone, which caused no increase in adrenal cyclic AMP, stimulated adrenal ornithine decarboxyase activity. These observations suggest that the increase in adrenal ornithine decarboxylase activity stimulated by ACTH is not dependent upon steroidogenesis, nor is it dependent on the early peak of cyclic AMP, although it may be influenced by the sustained levels of tissue cyclic AMP that follow the administration of large doses of ACTH. Furthermore, it appears there may be a pathway of ornithine decarboxylase activation in the adrenal which is entirely independent of cyclic AMP mediation. The effects of hypophysectomy on adrenal ornithine decarboxylase response to ACTH were examined. In rats given ACTH 16 h after hypophysectomy, the increase in ornithine decarboxylase activity was delayed when compared with the response in animals given ACTH 1 h after hypophysectomy. Actinomycin D given during the first 3 h after ACTH in the 16 h hypophysectomized rat abolished the expected increase in ornithine decarboxylase activity. Thereafter, a progressive increase in ornithine decarboxylase activity was observed as the interval between ACTH and Actinomycin D administration was further increased. In contrast, Actinomycin D administered 15 min before ACTH in the 1 h hypophysectomized rat had no effect on the subsequent increase in ornithine decarboxylase activity, and actually progressively enhanced the response the longer its administration after ACTH was delayed. Cycloheximide abolished the response to ACTH in both the 1 h and the 16 h hypophysectomized rat. Thus, it appears that ACTH stimulates a post-transcriptional mechanism regulating ornithine decarboxylase activity in the acutely hypophysectomized animal, whereas, in the chronically hypophysectomized rat, ACTH must first stimulate transcription of new messenger RNA which is involved in regulation of adrenal ornithine decarboxylase synthesis.

Adrenal Glands↗

PubMed1992

Expression of steroidogenic enzymes in the bovine placenta and fetal adrenal glands throughout gestation.

The expression of cholesterol side-chain cleavage cytochrome P450 (P450scc), 17 alpha-hydroxylase cytochrome P450 (P45017 alpha), and 3 beta-hydroxysteroid dehydrogenase (3 beta HSD) was studied in bovine placenta and fetal adrenal glands throughout gestation. The levels of expression of these enzymes were much lower in the placenta than in the adrenals by Western and Northern analyses. The levels of P450scc, however, remained relatively constant in bovine placenta and fetal adrenal glands at all gestational stages studied. In contrast, P45017 alpha expression was higher in both the placenta and the fetal adrenal glands during the early stages of pregnancy, but declined markedly in both tissues through the period of midgestation. The expression of P45017 alpha increased markedly in the fetal adrenal glands in late gestation. The levels of 3 beta HSD were extremely low in placental tissues, but were higher in the fetal adrenals, where they were found to be slightly elevated in early and late gestation compared to those in midgestational stages. Immunocytochemical examination of the levels of P45017 alpha and 3 beta HSD in the fetal adrenal glands correlated with the results of Western and Northern analyses. In addition, the morphology and distribution of these two enzymes in the developing bovine fetal adrenal glands indicated that while the early activated gland is functional relative to the ability to secrete steroids, structural and functional organization more typical of mature adrenal glands is not achieved until the time of activation of the fetal adrenals in late gestation.

3-Hydroxysteroid Dehydrogenases↗

PubMed1996

Molecular and functional characterization of V1b vasopressin receptor in rat adrenal medulla.

In rat adrenal medulla, PCR experiments reveal the expression of messenger RNA encoding the gene for the V1b vasopressin receptor. Complementary DNA amplified sequences corresponded to the cloned rat pituitary V1b vasopressin receptor. Video microscopy experiments performed on fura-2-loaded adrenal medullary or adrenal glomerulosa cell primary cultures showed that vasopressin dose dependently mobilized intracellular calcium, suggesting that functional vasopressin receptors are expressed in these tissues. The use of d[D-3-Pal]vasopressin, a specific V1b vasopressin agonist, and SR 49059, a specific V1b vasopressin antagonist, revealed that V1b receptors are exclusively expressed in adrenal medulla. Using an indirect immunological approach (plasma membrane localization of dopamine-beta-hydroxylase), we demonstrated that stimulation of rat adrenal medulla V1b receptor leads to catecholamine secretion. More interestingly, PCR experiments performed on rat adrenal medulla RNA revealed that the arginine vasopressin-encoding gene is also expressed in this tissue. In addition, perifusion experiments indicated that [Arg8] vasopressin is released by the adrenal medulla. Together, these data suggest that vasopressin may regulate the adrenal functions by paracrine/autocrine mechanisms involving distinct vasopressin receptor subtypes: V1a in the adrenal cortex and V1b in the adrenal medulla.

Adrenal Medulla↗