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PubMed2003

Effects of vasopressin on adrenal gland regional perfusion during experimental cardiopulmonary resuscitation.

OBJECTIVE: Despite the important role of the adrenal gland during cardiac arrest, little is known about changes in the adrenal medullary or cortical blood flow in this setting. This study was designed to assess regional adrenal gland perfusion in the medulla and cortex during cardiopulmonary resuscitation (CPR), and after administration of adrenaline (epinephrine) versus vasopressin versus saline placebo. METHODS: After 4 min of untreated ventricular fibrillation, and 3 min of basic life support CPR, 19 animals were randomly assigned to receive either vasopressin (0.4 U/kg; n=7), adrenaline (45 microg/kg; n=6) or saline placebo (n=6), respectively. Haemodynamic variables, adrenal, and renal blood flow were measured after 90 s of CPR, and 90 s and 5 min after drug administration. RESULTS: All values are given as mean+/-S.E.M. Blood flow in the adrenal medulla was significantly higher 90 s after adrenaline when compared with saline placebo in the right adrenal medulla (210+/-14 vs. 102+/-5 ml/min per 100 mg), and in the left adrenal medulla (218+/-14 vs. 96+/-3 ml/min per 100 mg). Blood flow in the adrenal medulla was significantly higher 90 s and 5 min after vasopressin when compared with adrenaline in the right (326+/-22 mg vs. 210+/-14 ml/min per 100 mg, and 297+/-17 vs. 103+/-5 ml/min per 100 mg), and in the left medulla (333+/-25 vs. 218+/-14 ml/min per 100 mg, and 295+/-14 vs. 111+/-7 ml/min per 100 mg). Ninety seconds and five minutes after vasopressin, and 90 s after adrenaline, adrenal cortex blood flow was significantly higher when compared with saline placebo. After 12 min of cardiac arrest, including 8 min of CPR, seven of seven pigs in the vasopressin group, one of six pigs in the adrenaline group, but none of six placebo were successfully defibrillated. CONCLUSION: Both vasopressin and adrenaline produced significantly higher medullary and cortical adrenal gland perfusion during CPR than did a saline placebo; but vasopressin resulted in significantly higher medullary adrenal gland blood flow when compared with adrenaline.

Adrenal Glands↗
PubMed1999

Species differences in adrenal lipid peroxidation: role of alpha-tocopherol.

Previous reports have noted high levels of lipid peroxidation (LP) in vitro in a variety of adrenocortical preparations. However, we have observed that susceptibility to adrenal LP seems to vary considerably from species to species. The current study was done to confirm these apparent species differences in adrenal LP in vitro and to determine if they were attributable to differences in alpha-tocopherol content. Incubation of mitochondrial or microsomal preparations from guinea pig or rabbit adrenal glands with ferrous ion (Fe2+) caused a time-dependent increase in the formation of thiobarbituric acid reactive substances (TBARS) accompanied by depletion of alpha-tocopherol. By contrast, incubation of adrenal mitochondria or microsomes from rats or monkeys with Fe2+ had little or no detectable effect on TBARS and basal adrenal alpha-tocopherol levels were five to ten-fold greater than those in guinea pigs or rabbits. In addition, there was little change in alpha-tocopherol concentrations during incubation of rat or monkey adrenal tissue. Dietary alpha-tocopherol deficiency in rats reduced adrenal alpha-tocopherol to concentrations approximating those in guinea pigs. Incubation with Fe2+ induced high levels of TBARS in adrenal mitochondria and microsomes from the alpha-tocopherol deficient rats. Conversely, dietary alpha-tocopherol supplementation in rabbits increased adrenal alpha-tocopherol levels and prevented Fe2+ induced TBARS formation in mitochondria and microsomes. The results indicate that there are large species differences in adrenal susceptibility to LP in vitro and that these differences are at least partly attributable to species differences in adrenal alpha-tocopherol concentrations.

Adrenal Cortex↗
PubMed2001

Is MRI more accurate than CT in estimating the real size of adrenal tumours?

BACKGROUND: The size of adrenal tumour plays an important role in the indications for surgical excision of non-functioning adrenal tumours and in selecting the best surgical approach. Computed tomography (CT) has been reported to underestimate the real size of adrenal lesions. The accuracy of magnetic resonance imaging (MRI) in predicting the true tumour size has not been previously investigated. The present retrospective study investigates the accuracy of MRI and CT in the pre-operative determination of true adrenal tumour size. METHODS: The medical records of 65 patients who underwent adrenalectomy for an adrenal mass were reviewed. The size of adrenal tumours as determined by pre-operative MRI and/or CT was compared with the "true" histopathological size. The impact of histological diagnosis on size estimation was also investigated. RESULTS: The median age at diagnosis was 42 years (range 1-82 years) and more patients were female (60%). Five patients had bilateral adrenalectomy, thus giving rise to 70 adrenal specimens. The histopathological size of adrenal tumours ranged from 0.9 to 26 cm with a mean of 5.96 cm and a median of 4.70 cm. For tumours larger than 3 cm, MRI significantly underestimated the real tumour size by 20% (P<0.001). CT also underestimated the size of such tumours by 18.1% (P<0.003). Adrenal phaeochromocytomas were consistently underestimated by both modalities. CONCLUSIONS: MRI and CT significantly underestimated the true size of adrenal tumours larger than 3 cm by 20% and 18%, respectively. Surgeons and endocrinologists should interpret the pre-operative size of adrenal lesions with caution.

Adolescent↗
PubMed1998

Endosonography of the adrenal glands: normal size--pathological findings.

Transabdominal sonography of the adrenal glands frequently is non-successful. It was the aim of this project to improve the imaging of the adrenal glands using high resolution sonography in order to obtain information about even small changes in these organs. Therefore, endosonographic imaging was investigated using an endosonoscope PENTAX FG32UA. The correct identification of the adrenal glands was examined in five human cadavers. A total of 58 patients with 113 adrenal glands (in 3 cases history of unilateral adrenalectomy) were investigated. 109 adrenal glands (97%) were identified and evaluated. Healthy adrenal glands are slightly hyperechoich and regarding their echogeneity comparable to other endocrine organs such as the testes or the thyroid. Adrenal size can be determined as largest cross sectional area and was found to be 216 +/- 93 mm2 right and 231 +/- 98 mm2 left. In the adrenal glands which could be imaged by endosonography, all findings detected by CT (n = 33) or MRI (n = 19) could also be demonstrated endosonographically. Additional information as compared to CT/MRI was obtained in 7 out of 33 and in 6 out of 19 patients. This concerns in particular differentiation between tumor and hyperplasia and detection of small adrenal adenomas. High resolution endosonography of the adrenal glands can provide information about adrenal gland morphology which cannot be obtained by any other diagnostic approach.

ACTH Syndrome, Ectopic↗
PubMed2004

The orphan nuclear receptor NGFIB regulates transcription of 3beta-hydroxysteroid dehydrogenase. implications for the control of adrenal functional zonation.

3beta-Hydroxysteroid dehydrogenase type 2 (HSD3B2) is a steroid-metabolizing enzyme that is essential for adrenal production of mineralocorticoids and glucocorticoids. Thus, HSD3B2 is expressed at high levels in the glomerulosa and fasciculata, where these steroids are produced. In contrast, the production of dehydroepiandrosterone (DHEA) and DHEA sulfate in the adrenal reticularis is inversely correlated with the expression of HSD3B2. The reasons for the zonal expression of HSD3B2 are not known but represent an important aspect in the biochemical zonation of the adrenal. Using microarray, real time reverse transcriptase-PCR, immunohistochemistry, and HSD3B2 promoter analysis, we demonstrate that the NGFIB family of nuclear hormone receptors plays a critical part in the regulation of HSD3B2 transcription and may play an important role in the functional zonation of the adrenal gland. Microarray analysis of cortisol- versus DHEA sulfate-producing adrenal tissue demonstrated that NGIFB paralleled expression of HSD3B2 with expression much higher in cortisol-producing adrenal tissue; this observation was also demonstrated using real time reverse transcriptase-PCR analysis. In addition, immunohistochemistry confirmed that within adult and fetal adrenal gland NGFIB expression paralleled expression of HSD3B2. Transient transfections into H295R adrenal cells demonstrated that NGFIB family members enhanced HSD3B2 reporter activity but had no effect on a 17alpha-hydroxylase (CYP17) promoter construct. Deletion and mutational analyses of the 5'-flanking region of the HSD3B2 gene identified a consensus NGFIB response element that bound NGFIB in mobility shift assays. Infection of cultured human adrenal cells with adenovirus-containing NGFIB increased cortisol production by 8-fold and increased expression of HSD3B2 mRNA 26-fold over that observed in mock-infected cells. In primary cultures of adrenal cells, ACTH, an activator of HSD3B2, rapidly induced expression of NGFIB. These results suggest that NGFIB plays a crucial role in adrenal zonation by regulating HSD3B2 gene transcription.

3-Hydroxysteroid Dehydrogenases↗
PubMed2002

The adrenal genetic puzzle: how do the fetal and adult pieces differ?

The basis for the steroidogenic differences between the human fetal adrenal (HFA) and adult adrenal is not well defined. However, gene expression clearly plays a critical role in defining their distinct steroidogenic and structural phenotypes. We used DNA microarrays to compare expression levels of several thousand transcripts between the HFA and adult adrenal gland. Gene profiling was done using seven independent microarrays that contained between 7075 and 9182 cDNA elements. Twenty-five transcripts were found to have a greater than 5-fold difference in expression between HFA and adult adrenals. The largest differences were observed for transcripts that encode insulin-like growth factor-II (IGF-II) (25-fold higher in HFA) and 3beta hydroxysteroid dehydrogenase (3betaHSD) (21-fold higher in adult). The vast majority of the 25 transcripts have not been studied with regard to adrenal function. We also determined the transcripts that had the highest signal intensities, which is an approximate measure of expression level, for both the fetal and adult adrenal RNA samples. The enzyme 24-dehydrocholesterol reductase, which is involved in cholesterol biosynthesis, exhibited the highest signal intensity for fetal adrenal RNA. For adult adrenal mRNA, the expression of 11beta-hydroxylase transcripts was found to have the highest signal intensity ranking. Overall, 10 of the top 20 highest signal intensities were similar for adult and fetal adrenal transcripts. The gene profile data for fetal vs. adult adrenal glands should provide valuable information that could help define mechanisms involved in adrenal growth and development.

Adrenal Glands↗
PubMed1992

Gonadal steroids modulate adrenal fasciculata 3 beta-hydroxysteroid dehydrogenase-isomerase activity in mice.

The observation that adrenal 3 beta-hydroxysteroid dehydrogenase-delta 5----delta 4-isomerase (3 beta HSD) activity is greater in females than in males of both C57BL/6J and C3H/HeJ inbred strains of mice led us to test the hypothesis that this enzyme's activity within the adrenal gland may be modulated by gonadal steroids. Two weeks after sham-operation or castration, no castration effect was seen in adrenal 3 beta HSD activity, but the sex difference had been eliminated in C57BL/6J animals. Gonadal steroids were replaced in castrated animals of both sexes of C57BL/6J and C3H/HeJ mice. Daily injections of androgenic steroids (testosterone propionate or dihydrotestosterone) decreased adrenal 3 beta HSD activity in both sexes of both strains of mouse. Although estradiol benzoate did not alter adrenal 3 beta HSD activity in either sex or strain tested when the activity was expressed on a per adrenal gland basis, it did inhibit adrenal 3 beta HSD activity when expressed on a per milligram of adrenal tissue basis in C57BL/6J but not in C3H/HeJ animals. Histochemical staining for 3 beta HSD and the relationship between adrenal weight and the cross-sectional area of the zona fasciculata suggested that the adrenal zona fasciculata was the target of the inhibitory effects of androgens on adrenal 3 beta HSD activity.

Adrenal Glands↗
PubMed1984

The relationship of I-131 6 beta-iodomethyl-19-norcholesterol (NP-59) adrenal cortical uptake to indices of androgen secretion in women with hyperandrogenism.

Dexamethasone suppression (DS) adrenal cortical scintigraphy has been shown to be useful in the detection of the adrenal pathology in women with hyperandrogenism. However, a relationship between adrenal cortical uptake of I-131 6 beta-iodomethylnorcholesterol (NP-59) and the level of adrenal androgen secretion has not been established. A retrospective analysis of DS adrenal scintiscans has been performed on 39 women with hirsutism and hyperandrogenism. In 14 patients with normal patterns of imaging, in vivo adrenal gland iodocholesterol uptake, calculated using a semi-operator-independent-computer algorithm, did not correlate with the excretion of urinary 17-ketosteroids (17-KS). In contrast, in 20 patients demonstrating abnormal bilateral early imaging patterns, adrenal gland NP-59 uptake correlated significantly with the level of urinary 17-KS excretion (r = 0.65, P less than 0.05). To date seven of these 20 patients have had confirmatory procedures documenting the adrenal glands as contributing sites of androgen secretion. A similar correlation with urinary 17-KS excretion was seen in five other patients with unilateral imaging patterns (r = 0.94, P less than 0.005), due to androgen-secreting adrenal cortical adenomas. No correlation between adrenal NP-59 uptake and plasma testosterone or dehydroepiandrosterone sulphate levels was observed in any of the groups. Thus, adrenal gland uptake of NP-59 under DS reflects a measure of androgen secretion in women with androgen excess.

17-Hydroxycorticosteroids↗
PubMed1999

Computed tomography evaluation of adrenal masses.

Computed tomography is the first line modality in the evaluation of patients with adrenal gland masses, and has the potential to be very accurate in the localization of adrenal gland masses in patients with diseases associated with hyperfunctioning conditions of the adrenal gland. Computed tomography allows a specific diagnosis of acute adrenal haemorrhage, adrenal myelolipoma, and adrenal cysts. It is also helpful in the assessment of patients with Addison's disease, particularly the subacute form secondary to granulomatous diseases. Quantitative evaluation of adrenal masses on unenhanced or delayed-enhanced computed tomography has been shown to be highly accurate in distinguishing adrenal adenomas from non-adenomas. Attenuation of 18 HU or less on unenhanced computed tomography scans indicates adenoma with a high specificity and acceptable sensitivity. On delayed-enhanced computed tomography scans, adrenal adenomas exhibit a greater washout of contrast material than do adrenal non-adenomas. Therefore, adrenal non-adenomas have significantly higher attenuation than adenomas on delayed-enhanced computed tomography scans obtained at arbitrarily chosen times (3-60 min) after the initiation of contrast material administration.

Adrenal Gland Diseases↗
PubMed1995

Increased expression of proopiomelanocortin (POMC) mRNA in adrenal glands of mice undergoing graft-versus-host disease (GVHD): association with persistent elevated plasma corticosterone levels.

GVHD in animal models induces severe thymic atrophy as a result of prolonged secretion of high concentrations of adrenal glucocorticoids. In this study we investigated the mechanism responsible for the persistent stimulation of the adrenal glands to secrete glucocorticoids in mice undergoing GVHD. GVHD was induced across the major and multiple minor histocompatibility antigen difference in unirradiated C57Bl/6 x AF1 hybrid mice by the intravenous injection of A strain parental lymphoid cells. Our results showed plasma corticosterone (CS) levels were elevated in association with high concentrations of corticotropin (ACTH) in both the GVHD and control syngeneic (SYN) groups on day 9. By days 16 and 24, plasma CS and ACTH in the SYN mice returned to basal levels. In contrast, plasma CS levels remained elevated in the GVHD animals on days 16 and 24 despite decreasing concentrations of plasma ACTH. Reverse transcription-polymerase chain reaction (RT-PCR) showed several-fold increase in POMC mRNA in the adrenal glands of GVHD mice compared with SYN animals. In addition, high mRNA levels for murine prohormone convertase 1, the enzyme that cleaves POMC into ACTH, were also detected in GVHD adrenals. Histological analysis of GVHD adrenals failed to show any sign of adrenalitis, and RT-PCR of GVHD adrenals also failed to detect mRNA for interferon-gamma (IFN-gamma), a cytokine expressed by activated T and natural killer (NK) cells. However, mRNA for IL-12, a cytokine produced by activated macrophages, was increased in GVHD adrenals, suggesting that resident adrenal macrophages were activated during GVHD. Our findings suggest that persistent elevated levels of plasma glucocorticoids during GVHD could be mediated by intra-adrenal ACTH produced by resident adrenal macrophages activated as a consequence of GVHD.

Adrenal Glands↗
PubMed2005

Proliferative activity and genetic changes in adrenal cortical tumors examined by flow cytometry, fluorescence in situ hybridization and immunohistochemistry.

BACKGROUND: To determine differences in biological features among different adrenal tumors, we investigated the DNA ploidy, numerical chromosomal aberration and proliferative activity in human adrenal cortical neoplasms. METHODS: Our study included six adrenal cortical adenomas with Cushing syndrome, 12 adenomas with hyperaldosteronism, three non-functioning adenomas and three adrenal cortical carcinomas. Isolated nuclei from frozen samples were used for fluorescence in situ hybridization (FISH) analysis, and formalin-fixed, paraffin-embedded tissues from the same materials were analyzed using flow cytometry (FCM) for DNA ploidy. Sections from paraffin blocks were stained immunohistochemically with antibodies against Ki-67 and p53. For FISH analysis, we used an alpha-centromeric enumeration probe for chromosome 17. RESULTS: The mean Ki-67 labeling index (LI) of adrenal cortical carcinomas was markedly higher than that of adrenal cortical adenomas (209.4 vs 8.7). In functional adrenal cortical adenomas, the LI was significantly lower in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004), although FCM results indicated that tetraploid patterns were more frequently observed in the former type. Tumor size was significantly smaller in adenomas with hyperaldosteronism than in those with Cushing syndrome (P = 0.004). Chromosome 17 showed disomy in all adrenal cortical adenomas, whereas chromosome 17 abnormalities were found in two of three adrenal cortical carcinomas. Only the latter two cases strongly expressed p53 protein. CONCLUSIONS: Our study characterized various biological features of benign and malignant adrenal cortical tumors. The use of a combination of markers might provide additional information to assist our understanding of the clinical behavior of an individual adrenal cortical tumor.

Adenoma↗
PubMed1971

Preferential secretion of adrenaline or noradrenaline by the cat adrenal in vivo in response to different stimuli.

1. The concentrations of adrenaline and noradrenaline in the adrenal vein and the adrenal gland of the cat were studied in response to different stimuli leading to increased catecholamine (CA) secretion.2. Haemorrhage and hypoglycaemia, but not acute exposure to cold or intravenous administration of cocaine, induced considerable increases in total catecholamine secretion.3. The ratio of the concentration of adrenaline to noradrenaline in adrenal vein plasma during the control period was higher than the ratio in the adrenal gland itself.4. Haemorrhage increased noradrenaline secretion considerably more than adrenaline secretion so that the ratio of the concentration of adrenaline to noradrenaline in adrenal vein plasma was significantly lower than in the adrenal gland itself.5. Hypoglycaemia induced by insulin increased catecholamine secretion, with the adrenaline to noradrenaline ratio significantly higher than in the adrenal gland itself.6. Hypothermia resulted in a fall of the initial high ratio of adrenaline to noradrenaline, to a value similar to that in the adrenal gland.7. Neither cocaine nor changes in adrenal plasma flow affected the adrenaline to noradrenaline ratio in adrenal vein blood.8. It is concluded that preferential release from the adrenal gland of either adrenaline or noradrenaline is possible in vivo in response to different stimuli.

Adrenal Glands↗
PubMed2001

Adrenal lipomatous tumours: a 30 year clinicopathological experience at a single institution.

AIMS: Fatty tumours of the adrenal gland are uncommon and their features have received little attention in the literature. The aim of this study is to analyse the features of adrenal lipomatous tumours. METHODS: The histological features of primary adrenal tumours reported over a 30 year period (1970 to 1999) in Queen Mary Hospital, Hong Kong were reviewed and the clinicopathological features of adrenal lipomatous tumours were analysed. RESULTS: Adrenal lipomatous tumours were noted in 20 patients (12 men, eight women), and they accounted for 4.8% of the primary adrenal tumours reported. The adrenal fatty tumours comprised 11 myelolipomas, three lipomas, three teratomas, two angiomyolipomas, and one liposarcoma. Calcification or bone was noted in one third (seven of 20) of the adrenal tumours. In some fatty tumours (myelolipoma and angiomyolipoma), the fatty component may be inconspicuous. This is the first report in the English literature of angiomyolipoma and liposarcoma of the adrenal gland. CONCLUSIONS: Different types of fatty tumours were noted in the adrenal gland. A high index of suspicion should be maintained with an aim of surgical treatment for selected patients with large and symptomatic adrenal lipomatous lesions. Histological confirmation is needed for diagnosis.

Adolescent↗
PubMed1998

Non-small cell lung carcinoma: usefulness of unenhanced helical CT of the adrenal glands in an unmonitored environment.

PURPOSE: To evaluate routine non-contrast material-enhanced helical computed tomography (CT) of the adrenal glands in patients with non-small cell lung carcinoma to facilitate characterization of adrenal masses detected in an unmonitored environment (i.e., the radiologist on duty did not look at the acquired images before the patient left the scanner). MATERIALS AND METHODS: One hundred consecutive patients with non-small cell lung carcinoma were referred for CT evaluation of the chest; chest and abdomen; or chest, abdomen, and brain. All underwent unenhanced CT of the adrenal glands before the requested CT examination. The morphologic features, size, and attenuation values of the adrenal masses were calculated. Attenuation values of adrenal masses from prior imaging, if available, were compared with those at follow-up imaging to classify these masses. Variable unit cost increase in obtaining these additional images was estimated. RESULTS: Fifteen adrenal masses were identified in 13 patients. In one patient, bilateral ill-defined adrenal masses were present. In 12 patients, 13 masses were sharply circumscribed: Seven were less than 10 HU and six were 20 HU or greater at unenhanced CT. Nine of these 12 patients received iodinated contrast material. Without the unenhanced CT, 10 adrenal masses in these nine patients would have been indeterminate for malignancy. In six of these nine patients, the adrenal mass was the only potential site of metastatic disease. The unenhanced CT data helped classify three of these masses as benign-10 HU or less- and three as indeterminate-greater than 10 HU. CONCLUSION: Unenhanced CT of the adrenal glands can prospectively characterize adrenal masses and obviate further examination in patients with lung carcinoma.

Adrenal Gland Neoplasms↗
PubMed1986

Sodium retention after adrenal enucleation.

Adrenal enucleation (removal of the adrenal gland, leaving the capsule intact) results in regeneration of the adrenal cortex. During the first 1-2 wk of adrenal regeneration, marked renal sodium avidity and positive sodium balance are noted. This renal sodium avidity appears mediated via adrenocorticotropin-stimulated secretion of a potent mineralocorticoid by the regenerating adrenal cortex. In this review, we have examined relationships between the histology and ultrastructure of the regenerating adrenal cortex, renal sodium handling, and adrenal steroid production at various times after the initiation of adrenal regeneration. Plasma levels of known mineralocorticoids are subnormal during the period of most intense sodium avidity, while urinary excretion of a potent mineralocorticoid, 19-nordeoxycorticosterone, has been found to be increased in rats with regenerating adrenals during this period of most intense sodium avidity. This hormone, however, is not elevated in rats with regenerating adrenals after resolution of the period of sodium avidity. In this article, we review the experimental evidence regarding the potency of this mineralocorticoid and its likely role in the sodium retention after adrenal enucleation.

Adrenal Glands↗
PubMed1977

Opposite effects of ACTH and glucocorticoids on adrenal DNA synthesis in vivo.

Administration of ACTH to rapidly growing weanling rats results in an increase of DNA synthesis in adrenal and a decrease in liver. Dexamethasone administration decreases both adrenal and liver DNA synthesis. When both hormones were administered to the same animals, the liver DNA synthesis was similar to that observed with dexamethasone alone, but the DNA synthesis in adrenal was lower than that obtained with ACTH alone, yet higher than that observed with dexamethasone. The plasma levels of corticosterone were similar in animals treated with ACTH or with ACTH plus dexamethasone. Aminoglutethimide stimulated adrenal DNA synthesis, but less than ACTH. This substance overcame partially the inhibitory effects of dexamethasone on liver DNA synthesis but did not in adrenal. When both ACTH and aminoglutethimide were given simultaneously, adrenal DNA synthesis was higher than that observed with each substance alone. In all experiments in which adrenal cytosol DNA polymerase was studied, the activity varied in the same direction as DNA synthesis. These results indicate opposing effects of ACTH and glucocorticoids on adrenal DNA synthesis. The finding of a glucocorticoid effect on the adrenal is supported by the demonstration of a glucocorticoid specific binding protein in adrenal cytosol. Cycloheximide blocks the stimulatory action of ACTH on both steroidogenesis and DNA synthesis. Actinomycin D, as well as dexamethasone, blocks only the DNA synthesis-promoting action of ACTH. This latter result suggests some differences in the metabolic pathways by which ACTH controls steroidogenesis and growth in the adrenal cell.

Adrenal Glands↗
PubMed1978

Converting enzyme inhibition augments and competitive inhibition of angiotensin II partially restores reflex adrenal catecholamine release in anephric dogs.

Adrenal epinephrine (E) release after hemorrhage in anesthetized dogs is blunted by acute nephrectomy and restored by angiotensin II infusion. In the present study, we report the effect of converting enzyme inhibition by SQ 20881, a decapeptide, and of competition inhibition of angiotensin II by saralasin (1-Sar-8-Ala-Ang-II) on reflexly stimulated adrenal release of E and norepinephrine (NE) in three groups of acutely anephric dogs. Aortic catheters and adrenal vein to femoral vein Silastic shunts were placed in dogs anesthetized with pentobarbital and mechanically ventilated. Adrenal secretion rates were calculated from adrenal vein to aorta catecholamine concentration differences divided by measured adrenal venous flow. Catecholamine concentrations were determined with trihydroxyindole technique. Blood samples were obtained before and 15, 30, and 60 min after rapid hemorrhage to a stable mean arterial pressure of 50 mm Hg. Saralasin infusion (10 microgram/kg/min) supported adrenal E release in anephric hemorrhaged dogs toward secretion rates comparable to those seen in intact dogs. Anephric SQ 20881 (approximately 0.5 microgram/kg) recipients had delayed (60 min) augmented adrenal E and NE release after hemorrhage. In resting animals not reflexly stimulated by hypovolemia, neither drug provoked adrenal E or NE release. These results suggest an agonist effect of saralasin on reflex adrenal E release and increased responsiveness of the stimulated adrenal medulla under the influence of converting enzyme inhibition.

Adrenal Medulla↗
PubMed1983

Relationships among adrenal weight, corticosterone, and stimulated adrenocorticotropin levels in rats.

Based on results of previous studies, we tested the hypothesis that increased adrenal weight in the absence of increased corticosterone secretion would inhibit the magnitude of the ACTH response to ether vapor. Adrenal hypertrophy was induced by treatment of rats for 3 days with aminoglutethimide, cyanoketone, or metyrapone, three agents that act to inhibit enzymes required for corticosterone synthesis. On the fourth day, resting plasma ACTH and corticosterone levels were normal; however, the logarithm of the ACTH response to ether was directly related to total adrenal weight. This result did not support the hypothesis. Unilateral adrenalectomy and treatment with cyanoketone resulted in total adrenal weight equivalent to that of control rats bearing two adrenals. Resting ACTH levels were normal, but stimulated ACTH was significantly greater in these rats than in controls or in rats with two adrenals, suggesting that there is an interaction between the effects of unilateral adrenalectomy and adrenal enzyme inhibition. As anticipated, adrenal hypertrophy with increased corticosterone production caused by ACTH infusion resulted in a significant negative relationship between resting and stimulated ACTH levels and adrenal weight. We conclude that when adrenals are enlarged by means that prevent excessive corticosterone secretion, there is a mechanism associated with the increase in adrenal weight that correlates directly with the magnitude of stimulated ACTH secretion. We have reexamined the results of our previous results in the light of these experiments.

Adrenal Glands↗