Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ADRENALS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed2006

Cu/Zn- and Mn-superoxide dismutase distribution and concentration in adrenal tumors.

The tissue distribution of Cu/Zn- and Mn-superoxide dismutases (SOD) in adrenal tumors was studied by an immunohistochemical technique, and the concentrations of both SODs were measured by a sensitive sandwich enzyme immunoassay technique. In the normal adrenal gland, both Cu/Zn- and Mn-SODs were localized predominantly in the reticular zone of the cortex. Cu/Zn-SOD was stained clearly in the inner fascicular zone of the cortex, but not in the medulla, whereas Mn-SOD was stained weakly in the medulla. In different adrenal tumors, the localization of both stained SODs reflected the origin of the tumor cell. Thus, in one section of a pheochromocytoma only Mn-SOD was stained clearly. The concentrations of both SODs in the tissues of medullary tumors were lower than those in the normal adrenal gland and adrenocortical adenomas. The concentration of Cu/Zn-SOD in the tumor tissue of Cushing's syndrome adenoma was higher, and that of Mn-SOD was lower than the concentrations in the normal adrenal gland. The ratio of the tissue concentrations of Mn-SOD to Cu/Zn-SOD was lower in adrenal medullary tumors and Cushing's syndrome adenomas than in the normal adrenal gland and primary aldosteronism adenomas, indicating the predominance of Cu/Zn-SOD in the former, and Mn-SOD in the latter. These data suggest that the localization of Cu/Zn- and Mn-SODs in adrenal tissues reflects the specificity of the adrenal cells that produce the tissue-specific hormones. An investigation of changes in these enzymes in adrenal tumors may also provide useful information on adrenal tumor cell differentiation.

Adrenal Cortex↗
PubMed2003

The effect of a steroid "burst" and long-term, inhaled fluticasone propionate on adrenal reserve.

BACKGROUND: Although widely used, the effects of steroid "bursts" on the hypothalamic-pituitary-adrenal axis, especially with long-term, concomitant topical steroids use, have not been studied. OBJECTIVE: To examine the effect of a prednisone burst, long-term intranasal steroids, and inhaled fluticasone propionate on the suppression and recovery of adrenal function. METHODS: Adult patients taking long-term intranasal steroids, either moderate-dose (440 microg/d) or high-dose (880 microg/d) inhaled fluticasone propionate, underwent a low-dose cosyntropin stimulation test (LDCST) before and 2 days after a prednisone burst. Suppressed adrenal responses were monitored with a weekly LDCST. Persistent abnormal LDCST results were confirmed by 8-hour cosyntropin infusion. Inhaled fluticasone dosages were decreased; adrenal recovery was evaluated by a monthly LDCST. Adverse effects of steroids were monitored by questionnaires. RESULTS: Sixty-three patients participated in the study. Three of 31 patients not taking inhaled steroids and 1 of 13 patients taking moderate-dose fluticasone had abnormal LDCST results on day 2 after the prednisone burst, which normalized by the second week. In the high-dose fluticasone group, 14 of 19 patients had suppressed LDCST responses on day 2 and adrenal function recovered in 10 of 19 patients by the fourth week. These patients complained significantly of decreased libido (P = 0.02), listlessness (P = 0.03), and weight loss (P = 0.05). High-dose fluticasone (r = 0.66, P < 0.001) and duration of use (r = 0.32, P = 0.01) were statistically correlated with adrenal impairment. Of the 4 patients with persistent adrenal impairment, 3 patients successfully reduced dosages of inhaled fluticasone and adrenal function recovered in 2 to 10 months. CONCLUSIONS: Prednisone bursts induce brief adrenal impairment. Intranasal steroids and moderate-dose fluticasone had no effect on adrenal function. High-dose, inhaled fluticasone caused mild-to-significant adrenal suppression and delayed the recovery after a steroid burst. Avoiding or limiting the duration of high-dose inhaled steroids would minimize systemic adverse effects.

Administration, Intranasal↗
PubMed1999

Functional capacity of fetal zone cells of the baboon fetal adrenal gland: a major source of alpha-inhibin.

We have shown that ACTH receptor mRNA expression and steroidogenesis were increased in the transitional zone and decreased in the fetal zone of the baboon fetal adrenal in the second half of gestation. Thus, we proposed that there is a divergence in ACTH receptor-mediated zone-specific steroidogenesis within the fetal adrenal during mid to late gestation. We have also demonstrated that fetal serum alpha-inhibin levels decline with advancing development. It is possible, therefore, that the alpha subunit of inhibin provides a good marker of fetal zone cellular function and that the changes in circulating fetal alpha-inhibin with advancing pregnancy reflect ontogenetic changes in fetal adrenal cortical zone-specific cell function. However, it remains to be determined whether the fetal adrenal is a major source of circulating alpha-inhibin in the fetus and whether alpha-inhibin is expressed in the fetal, definitive, and/or transitional zones. Therefore, the current study compared fetal serum alpha-inhibin levels with immunocytochemical localization of alpha-inhibin in baboon fetal adrenals obtained on Days 60 (early), 100 (mid), and 165 or 182 (late) of gestation (term averages Day 184) from animals untreated or treated with betamethasone, which we previously demonstrated suppressed fetal pituitary ACTH and adrenal weight. Fetal serum alpha-inhibin levels (mean +/- SE) were greater (p < 0.05) at mid (5863 +/- 730 microliter eq/ml) than at late (3246 +/- 379) gestation and were reduced (p < 0. 05) by betamethasone. The inhibin alpha subunit was expressed in abundant quantities in the fetal adrenal cortex, but not in medulla, throughout gestation. At mid and late gestation, alpha-inhibin was expressed throughout the fetal adrenal cortex but most intensely in the innermost area of fetal zone cells. By late gestation, the fetal adrenal exhibited a gradient of alpha-inhibin expression. Thus, the outermost definitive zone cells were devoid of alpha-inhibin, the transitional zone exhibited a relatively low alpha-inhibin content, and fetal zone cells continued to exhibit extensive expression of alpha-inhibin. Betamethasone diminished the intensity of alpha-inhibin expression throughout the fetal adrenal cortex. These results indicate that the fetal adrenal fetal zone is a significant source of circulating alpha-inhibin in the baboon fetus and that alpha-inhibin provides a good marker to study the developmental regulation of fetal zone-specific adrenocortical function.

Adrenal Cortex↗
PubMed2001

Adrenal insufficiency during the late stage of polymicrobial sepsis.

OBJECTIVES: Although studies have indicated that adrenal insufficiency occurs after severe trauma and hemorrhagic shock, it remains controversial whether adrenal function is depressed during the late stage of polymicrobial sepsis. DESIGN: Prospective, controlled animal study. SETTING: A university research laboratory. SUBJECTS: Male rats (275-325 g) were subjected to polymicrobial sepsis by cecal ligation and puncture (CLP) or sham operation followed by the administration of normal saline solution. MEASUREMENTS AND MAIN RESULTS: Systemic blood samples were taken at 20 hrs after CLP (i.e., a late stage of sepsis) or sham operation to measure plasma levels of corticosterone and corticotropin as well as adrenal contents of corticosterone. Additional groups of animals were utilized to examine corticotropin-stimulated plasma corticosterone release as well as adrenal levels of cyclic adenosine monophosphate (cAMP, the second messenger of corticotropin action). The results indicate that despite a 75% (p < .05) higher concentration in plasma corticotropin at 20 hrs after the onset of sepsis, plasma corticosterone levels were similar to those in sham-operated animals. In addition, adrenal contents of corticosterone were reduced by 42% (p < .05) in septic animals. Moreover, the plasma corticosterone and adrenal cAMP responses to corticotropin were reduced by 53% and 27% (p < .05), respectively, at 20 hrs after CLP. CONCLUSIONS: These findings suggest that, despite high plasma levels of endogenous corticotropin, adrenal dysfunction, as indicated by the reduction of corticotropin-induced plasma corticosterone release and adrenal contents of cAMP as well as the decreased adrenal levels of corticosterone, occurs during the late stage of polymicrobial sepsis. Therefore, the recognition of adrenal insufficiency and interventions to improve adrenal responsiveness may be beneficial in improving the outcome during late sepsis.

Adrenal Glands↗
PubMed1987

Adrenal gland: MR imaging.

The authors investigated the utility of magnetic resonance (MR) imaging in identifying the normal adrenal gland in 100 patients as well as in distinguishing adrenal adenomas (n = 12) from malignant neoplasms (n = 14). The left adrenal gland was seen in 99 of 100 cases and the right in 91 of 100 cases. The adrenals were most easily seen with T1-weighted spin-echo pulse sequences. The ratio of the intensity of the adrenal mass to that of fat at 2,100/90 (repetition time msec/echo time msec) was most helpful in distinguishing adrenal adenomas from malignant neoplasms. In contrast to other studies, the adrenal mass/liver intensity ratios were not helpful. All ten lesions with adrenal mass/fat ratios at 2,100/90 of 0.8 or greater were malignant, whereas all eight adrenal masses with a ratio less than 0.6 were adrenal adenomas. However, eight (31%) of the masses (four adenomas and four malignant neoplasms) had ratios between 0.6 and 0.8. Although MR imaging has considerable potential in characterizing adrenal masses, larger studies are needed to determine its true sensitivity and specificity.

Adenoma↗
PubMed1983

Drug-induced adrenal hypertrophy provides evidence for reset in the adrenocortical system.

These studies were performed to determine how bilateral adrenal hypertrophy persists despite normal resting ACTH levels in male rats for weeks after a 3-day course of treatment with cyanoketone (CK). This drug blocks corticosterone synthesis by binding to the enzyme 3 beta-ol-dehydrogenase-delta 5, delta 4-isomerase (EC 1.1.1.51). Although plasma ACTH levels were significantly elevated at all times during the course of treatment with CK, ACTH and corticosterone levels of CK-treated rats were normal thereafter compared to those in control rats killed in the morning. Despite these normal ACTH levels, adrenal weight remained elevated (by 100%) for at least 14 days. We determined that increased ACTH secretion was required to initiate and maintain the adrenal growth response to CK. Rats pretreated with hypophysectomy or dexamethasone (1 mg/kg) did not respond with increases in adrenal weight after CK treatment. Sustained elevations in ACTH during CK treatment were required for increased adrenal weight, because rats treated with dexamethasone 3 h after CK injection did not have enlarged adrenals at 24 h. Increased adrenal weight was not sustained after removal of supranormal levels of ACTH achieved by infusion, suggesting that after adrenal hypertrophy is achieved by ACTH, elevated ACTH levels are also required to maintain adrenal enlargement. Finally, ACTH and corticosterone levels were measured in the evening (at the peak of the diurnal rhythm in the adrenocortical system of rats) in CK-treated rats. Evening ACTH levels were significantly elevated in CK-treated rats compared to those in controls 7, 10, and 14 days after the onset of 3 days of treatment with CK; however, corticosterone levels were normal. The effects of CK on the adrenocortical system were exerted via the adrenal, since adrenalectomy normalized the amplitude of the diurnal rhythm of ACTH in CK-treated rats compared to that in adrenalectomized controls. We conclude 1) that adrenal hypertrophy after CK is maintained by increased ACTH secretion which occurs daily in the evening; and 2) that the results provide evidence for a daily reset of the corticosteroid feedback sensor in the adrenocortical system. This conclusion arises from the findings that there is a normal rhythm in corticosterone levels in CK-treated rats and that morning ACTH levels are normal although evening ACTH levels are significantly elevated.

Adrenal Cortex↗
PubMed2000

Up-regulation of adrenal cortical and medullary atrial natriuretic peptide and gene expression in rats with deoxycorticosterone acetate-salt treatment.

Our previous study demonstrated that human adrenal medulla is a site of atrial natriuretic peptide (ANP) synthesis. To further evaluate the role of adrenal ANP in body fluid homeostasis, we investigated the changes in adrenal ANP in rats receiving deoxycorticosterone acetate (DOCA)-salt treatment. In situ hybridization and immunohistochemical study showed that adrenal ANP messenger RNA (mRNA) and ANP-like immunoreactivities (ANP-LI) were mainly localized in the zona glomerulosa and medulla of vehicle-treated rats. DOCA-salt treatment activated ANP mRNA and peptide expression in all adrenal zones, especially in the zona fasciculata/reticularis from 12 h to the entire 8-day study period. Using a semiquantitative RT-PCR technique, the relative quantities of ANP mRNA in the adrenals of the DOCA-salt-treated group were significantly increased from 1 to 8 days, whereas the adrenal weights of DOCA-salt-treated rats were significantly decreased from day 2 to day 8. Our results are the first to indicate that ANP is synthesized not only in the adrenal medulla but also in the adrenal cortex and their syntheses are markedly increased in DOCA-salt-treated rats. These results imply that adrenal ANP may participate in the intraadrenal regulation of adrenal function on water-electrolyte homeostasis in an autocrine or paracrine manner.

Adrenal Cortex↗
PubMed2006

Adrenal tuberculosis in Cushing's disease with bilateral macronodular adrenocortical hyperplasia.

Cushing's disease is a disorder of hypercortisolism caused by a pituitary micro- or macro-adenoma. Most patients with Cushing's disease have a bilateral adrenal enlargement, which depends on the duration of the disease, as a result of the long standing ACTH stimulation of both adrenal glands. However, in macronodular adrenocortical hyperplasia (MNH) that is caused by Cushing's disease, if the MNH gains autonomy, a bilateral adrenalectomy, as well as the removal of pituitary adenoma, is often essential. We encountered a patient diagnosed with Cushing's disease with bilateral adrenal tuberculosis simulating MNH. She had taken anti-tuberculosis medications one year prior to admission due to spinal tuberculosis. Sellar MRI revealed a pituitary macroadenoma, but adrenal CT showed enlargement in both adrenal glands that appeared to be MNH. A hormonal study and bilateral inferior petrosal sinus sampling revealed Cushing's disease. Therefore, she underwent trans-sphenoidal surgery of the pituitary mass. The pituitary surgery was successful and the serum cortisol returned to normal range. However, the adrenal mass rapidly enlarged after removing the pituitary tumor without showing evidence of a recurrence or adrenal autonomy of hypercortisolism. Accordingly, a laparoscopic left adrenalectomy was performed to examine the nature of the mass. The resected left adrenal gland was pathologically determined to have a lesion of tuberculosis with some part of the intact cortex. So we assumed that the cause of rapid adrenal enlargement might be due to adrenal tuberculosis. In summary, to the best of our knowledge, this is the first case of Cushing's disease coexisting with both adrenal tuberculosis simulating a bilateral MNH.

Adrenal Gland Diseases↗
PubMed1995

Adrenal androgen production in polycystic ovary syndrome.

Secondary PCOS may occur in association with disorders characterized by adrenal androgen excess, e.g. congenital adrenal hyperplasia. Primary PCOS is associated frequently with more subtle abnormalities in adrenal androgen status. However, it has not been established that the mild adrenal androgen occurring in PCOS is causally involved in the development of PCOS, although adrenal hyperresponsiveness to stimulation appears to be characteristic of PCOS. It remains to be clarified whether this is due to excess stimulation of the adrenal by the putative CASH, which with ACTH probably coordinates adrenal androgen steroidogenesis, or whether adrenal hyperresponsiveness occurs as a consequence of increased cortisol clearance with compensatory hypersecretion of ACTH, which is associated with excessive adrenal androgen production. The possibility also exists that the enzyme system responsible for 17-hydroxyprogesterone production and its conversion to androgens is excessively active and may occur as a common defect in the adrenal and ovaries as a consequence of a congenital disorder. For at least some patients, treatment with a nocturnal low-dose glucocorticoid is an effective form of treatment. Indeed, this is the only hormonal form of treatment for hirsutism that also facilitates fertility and pregnancy. It is possible that PCOS may occur as a consequence of any disorder in which anovulation is associated with normal or elevated oestrogen levels. For some patients with PCOS, mild adrenal androgen excess is probably primary to development of the disorder. Thus, a trial of treatment with low-dose glucocorticoid at night appears to be a reasonable option in susceptible patients who can probably be recognized by demonstration of an excessive androgen response to ACTH or metyrapone.

Adrenal Glands↗
PubMedDate not supplied

[Vascular cysts of the adrenals. Association with aneurysm of the abdominal aorta].

A rare case of an adrenal vascular cyst associated to an abdominal aorta aneurysm is reported. Adrenal cysts are an uncommon clinical finding, in most cases incidentally discovered for nonspecific abdominal pain, during US, TC or RM evaluation or at autopsy. Small adrenal mass are clinically silent. They may be symptomatic (lumbar tension, pain) for dimensions over 10 centimetres. Cysts of large size can cause displacement and compression of adjacent organs. They present a difficult problem of differentiation between benign and malignant lesions. Non-neoplastic adrenal cysts have been divided into four categories: parasitic (7%), epithelial (9%), endothelial (45%) and haemorrhagic or pseudocystic (39%). Vascular adrenal cysts may be a traumatic consequence of an hamartomatous vascular anomaly. The aim of this paper is to discuss, on the basis of the literature, the etiology, diagnosis and treatment of the adrenal mass. Surgical timing is discussed for the concomitant vascular lesion. The elective treatment was left adrenalectomy performed through transperitoneal approach. Surgery for abdominal aorta aneurysm was differed because the adrenal mass was suspected to be an infected neoplastic lesion and for the feasibility of endovascular procedure. The adrenal specimens contained a cystic structure with fluid blood, fibrin and calcifications. Normal adrenal cortical tissue was found in the cystic wall. This lesion (arising from vascular anomalies) require separation from haemorrhagic adrenal neoplasm. Awareness of adrenal pseudocysts and careful attention to the hystological features aids this distinction.

Adrenal Gland Diseases↗
PubMed2002

[Pheochromocytomas as adrenal gland incidentalomas].

Adrenal incidentalomas are a heterogeneous group of pathological entities, including benign or malignant adrenocortical or medullary tumors, hormonally active or inactive lesions, which are identified incidentally during the examination of nonadrenal-related abdominal complaints. About 1.5% to 23% of adrenal incidentalomas are pheochromocytomas. Composite pheochromocytoma is a rare tumour of adrenal medulla with divergente clinical course. This type of pheochromocytoma is designated "composite" or "mixed," depending on whether pheochromocytoma and nonpheochromocytoma components show the same embryologic origin. Nonpheochromocytoma components found in the composite pheochromocytoma include ganglioneuroma, ganglioneuroblastoma, neuroblastoma, and malignant schwannoma. The biologic behavior of composite pheochromocytomas may be as difficult to predict as more traditional pheochromocytomas; based on the number of cases reported to date the presence of areas resembling ganglioneuroblastoma or neuroblastoma does not necessary indicate a poor prognosis. Some may behave in a malignant fashion with metastasis by a component of the tumour which has neural features. Pheochromocytomas and paragangliomas are well-defined entities. Some of their nonsporadic associations and unusual morphological appearances are not universally appreciated. We report on a rare association of left adrenal CP, with typical right adrenal phochromocytoma and retroperitoneal paraganglioma, and a review of literature. We analyzed the clinical and immunohistochemical features in a 24-year-old woman with composite pheochromocytoma localized in the left adrenal gland and associated with blood pressure of 200/140 mmHg. Abdominal computed tomography and 131-J MIBG revealed a 65 x 60 mm mass in the right adrenal gland, but no revealed 45 x 40 mm retroperitoneal mass and 20 x 20 mm mass in the left adrenal region. Serum and urinary adrenaline levels were high, and catecholamine levels in the blood sample of the selective adrenal vein, were also high. Bilateral adrenalectomy and retroperitoneal mass were surgically removed without complications. Clinical symptoms were absent 6 years after surgery. After surgery the patient gave birth to two healthy babies. Immunohistochemical analyses revealed that tumour cells of right adrenal pheochromocytoma and retroperitoneal paraganglioma were strongly positive for neurone specific enolase, synaptophisin and chromogranin A. The left adrenal tumour showed pheochromocytoma, ganglioneuroma and neuroblastoma components. Immunoreactivity of this tumour added several features to the wide immunohistochemical spectrum. This case demonstrates the indolent behavior of sporadic-type CP and retroperitoneal paraganglioma in an adult patient. Unusual morphological features of CP occur in a substantial number of cases and may cause diagnostic problems.

Adrenal Gland Neoplasms↗
PubMed1991

Renin in adrenal: an overview of its synthesis, subcellular localization, and functions.

Specific renin has been identified in the outer layers of the adrenal of rat, mouse and human. Nephrectomy causes a marked elevation of adrenal renin, presumably through hyperkalemia. The subcellular distribution of adrenal renin was investigated by Percoll density gradient. The renin activity in the dense granules from the capsules of nephrectomized rats was 15 times greater than that of intact rats. Most of the active form renin was found in the dense renin granules. Immunohistochemical studies revealed that the dense granules increased in number after bilateral nephrectomy. Immunogold staining of these granules showed unequivocally the presence of renin therein. Adrenal capsules in organ culture were found to release renin at a steady rate. Renin release from bilaterally nephrectomized rat adrenals was 4.6 times greater than from the organs of intact animals. Further, adrenal slices from human adrenocortical tumor tissues which contained specific renin in a sizable quantity were found to release renin in a similar fashion to rats. The mechanism of the control of renin secretion from the adrenal gland was different from the kidney in that the release was stimulated by potassium chloride or angiotensin II but not by ACTH, suggesting stimulation by intracellular calcium. These results provide convincing evidence that the adrenal synthesizes renin, stores it in specific secretory granules, and secretes it in a regulated manner. It is most likely that the adrenal renin plays a role in the production of aldosterone in the adrenal cortex or in the secretion of catecholamines from the adrenal medulla through intra- and/or extracellular formation of angiotensin II.

Adrenal Cortex↗
PubMed1982

Acute adrenal insufficiency: recognition, management, and prevention.

Acute adrenal insufficiency may present only with nonspecific symptoms and signs. Hyperpigmentation is not a feature of secondary adrenal insufficiency and is absent in patients with primary adrenal failure of recent or acute onset. Similarly, characteristic electrolyte disturbances may be obscured by concomitant vomiting and diarrhea as well as by parenteral electrolyte replacement. A high index of suspicion must therefore be maintained to make the diagnosis of acute adrenal insufficiency in patients without a recognized history of autoimmune adrenal insufficiency or of other diseases or therapeutic regimens known to result in pituitary-adrenal failure. Timely intervention with volume and glucocorticoid replacement rapidly reverses all symptoms and signs of adrenal insufficiency. Guidelines are presented for glucocorticoid replacement in the treatment of adrenal crisis as well as for the prevention of acute adrenal insufficiency in patients with known or suspected pituitary-adrenal disease. In addition, recommendations are given for the simultaneous diagnosis and treatment of adrenal insufficiency in patients without previously established disease.

Acute Disease↗
PubMed1994

Hepatic lipase gene is transcribed in rat adrenals into a truncated mRNA.

Rat adrenals contain a lipase activity that is indistinguishable from hepatic lipase (HL) present in liver. Expression of HL mRNA in adrenals was studied using the method of reverse transcription-polymerase chain reaction (RT-PCR). A 596-bp fragment of HL cDNA spanning exons 5 to 8 was amplified when using total RNA from rat adrenals and liver, but not from heart or kidney. The abundance of HL mRNA was quantified by competitive RT-PCR using a standard RNA that was generated in vitro by transcription from a deleted HL cDNA construct. Adrenals contained 0.4 attomoles of HL mRNA per microgram of total RNA, compared to 16 attomoles in liver. In hypertrophic adrenals isolated from corticotrophin-treated rats, the abundance also amounted to 0.4 attomoles of mRNA per microgram of total RNA. However, amplification of full-length cDNA from either control or hypertrophic adrenals was never observed. Detailed analysis by PCR using different combinations of primers indicated that exons 3 to 9 including the 3'-untranslated region were expressed in adrenal RNA, but not the first two coding exons. The upstream part of the adrenal lipase mRNA was cloned after rapid amplification of cDNA ends (RACE). The resulting clones showed a unique 126-bp sequence 5' of the exon 2-exon 3 junction. This sequence contained multiple termination codons in all three reading frames but lacked a potential start codon. RT-PCR using an HL-specific primer and an oligonucleotide directed against this 5'-sequence showed that it is not only expressed in RNA from adrenals but also in liver. Pulse-labeling of freshly isolated adrenocortical cells with [35S]methionine followed by immunoprecipitation with anti-HL antibodies failed to show synthesis of mature HL, but indicated the synthesis of immunoreactive proteins in the 40-45 kDa range that remained mainly intracellular. Hence, the HL gene is transcribed in adrenals but results in an mRNA species with a unique 5'-end. Translation from an internal start site may produce an intracellular HL isoform that differs markedly from the liver-type lipase previously identified in adrenals.

Adrenal Cortex↗
PubMed1998

Consequences of prenatal morphine exposure on the hypothalamo-pituitary-adrenal axis in the newborn rat: effect of maternal adrenalectomy.

The hypothalamo-pituitary-adrenal axis is already functional in rat fetuses in late gestation. We have reported previously that prenatal morphine exposure induced a severe atrophy of the adrenals and a decrease of corticosterone release in newborn rats at birth and during the early postnatal period. The first aim of the present study was to determine the effects of prenatal morphine exposure (1) on corticotrophin releasing factor (CRF) content of the hypothalamus, CRF immunofluorescence in the median eminence, CRF mRNA in the paraventricular nucleus (PVN) and pro-opiomelanocortin (POMC) mRNA in the anterior pituitary gland; (2) on CRF-induced ACTH release from the anterior pituitary gland in vitro; and (3) on ACTH-induced corticosterone release by the adrenals in vitro. Moreover, as morphine is a hepatotoxic factor, we determined the effects of prenatal morphine on liver weight and plasma corticosteroid binding globulin (CBG) binding capacity in newborn rats. Since acute administration of morphine stimulates corticosterone secretion in adult rats and since maternal corticosterone can cross the placental barrier, we also measured both adrenal weight and glucocorticoid activity in newborns from adrenalectomized mothers treated with morphine. The present results show that prenatal morphine given to intact mothers induced adrenal atrophy and hypoactivity in newborns but did not affect the responsiveness of the anterior pituitary gland to CRF or that of the adrenal gland to ACTH. Prenatal morphine reduced both CRF content in the newborn hypothalamus and CRF immunofluorescence in the median eminence without a significant effect on CRF mRNA expression in the PVN. Moreover, morphine induced a significant decrease of POMC mRNA in the anterior pituitary gland. However, morphine did not significantly affect the weight of the liver, or the plasma CBG binding capacity for corticosterone, in rat pups. In contrast, morphine treatment of the adrenalectomized mothers did not induce adrenal atrophy in newborns and did not impair adrenal activation during the early postnatal period. Maternal adrenalectomy also prevented the effects of prenatal morphine on hypothalamic content of CRF, CRF immunofluorescence in the median eminence, and POMC mRNA in the anterior pituitary gland. However, adrenal atrophy was observed at term in newborns of adrenalectomized mothers treated with both morphine and corticosterone or only corticosterone. In conclusion, morphine given to pregnant rats induced inhibition of the hypothalamo-pituitary-adrenal axis in pups at term. As maternal adrenalectomy prevented these effects, we speculate that an adrenal factor of maternal origin, probably corticosterone, mediated these drug effects on newborns.

Adrenal Glands↗
PubMedDate not supplied

The involvement of innervation in the regulation of fetal adrenal steroidogenesis.

Over the last decade, great interest has been generated in evaluation of the extent of neural control of the adrenal cortex and in adrenal cortical/medullary paracrine interactions. The purpose of this review is to summarize current knowledge of fetal adrenal cortical innervation and to present an overview of those studies of fetal adrenal function indicating that adrenal innervation plays a functional role in the control of glucocorticoid secretion under basal conditions and in response to a variety of homeostatic challenges. It will be helpful in understanding both the innervation of the adrenal cortex and the role of adrenal innervation in steroidogenesis during fetal development to briefly review experimental studies that have shed light on adrenal steroidogenesis during postnatal life. This is helpful for two reasons: 1) the vast majority of studies of adrenal innervation and its effect on steroidogenesis have utilized postnatal animals and 2) since the fetus is preparing for postnatal life, evaluating the level of function achieved postnatally provides crucial insights into the developmental stages of adrenal innervation and its role in steroidogenesis in preparing the fetus for an independent postnatal existence.

Adrenal Cortex↗
PubMedDate not supplied

Differential expression of prolactin receptor (PRLR) in normal and tumorous adrenal tissues: separation of cellular endocrine compartments by laser capture microdissection (LCM).

PRL stimulates adrenal steroidogenesis. In this study, we compared the PRLR expression in normal and tumorous adrenal tissues and investigated a potential proliferative effect of PRL in adrenal cells. mRNA expression of long and intermediate forms of PRLR was detected in both normal adrenal cortex as well as benign and malignant adrenal tumors and in the human adrenocortical carcinoma cell line NCI-H295. Molecular analysis of cells procured by LCM clearly demonstrated that PRLR mRNA is expressed in the adrenal cortex but not in the medulla. Immunostaining revealed PRLR protein in all three zones of the normal adrenal cortex. Furthermore, adrenal carcinomas and adenomas stained positive for the PRLR, while in phaeochromocytomas as in the normal adrenal medulla, no specific staining was observed. By WST-1 test, we could show that PRL (10(-7) M) decreased proliferation and viability of adrenal cells in primary cell culture suggesting that PRL is not a mitogenic factor of adrenocortical cells.

Adrenal Cortex↗
PubMed1994

Adrenal size is increased in multiple sclerosis.

OBJECTIVE: To determine if adrenal glands are enlarged in multiple sclerosis (MS). Patients with MS and major depression are insensitive to glucocorticoid feedback regulation. Depressed patients have excessively high glucocorticoid levels and enlarged adrenal glands. To our knowledge, this is the first study of adrenal size in MS. Chronic high levels of adrenal glucocorticoid in MS may downregulate responses to exogenous or endogenous steroids. DESIGN: Retrospective postmortem analysis compared adrenal size in MS with that in other neurologic and non-neurologic diseases. SETTING: Autopsy cases were obtained from the records of a tertiary care hospital. PATIENTS: Ten patients had definite MS; 13, amyotrophic lateral sclerosis; and 14, acute myocardial infarction. MAIN OUTCOME MEASURES: Adrenal and body weight at autopsy. RESULTS: At postmortem examination, the adrenal glands of patients with MS were enlarged in comparison with the adrenal glands of patients who died of acute myocardial infarction or amyotrophic lateral sclerosis. The adrenal glands of the patients with MS were 36% larger than those of the patients with amyotrophic lateral sclerosis who had comparable body weights. The adrenal-body weight ratio was 40% greater in patients with MS than in patients who died of acute myocardial infarction. CONCLUSIONS: The increased adrenal size in patients with MS may allow excessive glucocorticoid secretion in response to stress and affect immune regulation.

Adrenal Glands↗