Showing papers on "Adrenal cortex published in 1971"

Clinical chemistry in diagnosis and treatment

Abstract: The kidney - renal calculi sodium and water metabolism potassium metabolism - diuretic therapy hydrogen ion homeostasis - blood gas levels the hypothalamus and pituitary gland adrenal cortex - ACTH the reproductive system - pregnancy thyroid function - TSH calcium, phosphate and magnesium metabolism carbohydrate metabolism and its interrelationships plasma lipids and lipoproteins intestinal absorption - gastric and pancreatic function vitamins liver disease and gall stones plasma enzymes in diagnosis proteins in plasma and urine clinical chemistry of the newborn inborn errors of metabolism purine and urate metabolism iron metabolism the porphyrias biochemical effects of tumours the cerebrospinal fluid drug monitoring the clinician's contribution to valid results requesting tests and interpreting results.

Long-term trophic effect of ACTH on rat adrenocortical cells. An ultrastructural, morphometric and autoradiographic study.

Abstract: The changes occurring in rat adrenocortical cells (zona fasciculata) during an 8 day period of treatment with ACTH, were investigated by morphometric and autoradiographic methods. The most important ultrastructural change consists in a conspicuous increase in the smooth endoplasmic reticulum, that accounts for about 50% of the total increase of cellular volume. Also the mitochondrial fraction shows a significant increase, which is found to be due both to the increment in the number of mitochondria per cell and to the increase in the mean volume of organelles themselves. The quantitative autoradiographic data, indicating an increment in the incorporation of 3H-orotate and 3H-leucine into adrenocortical cells of the treated animals, allow us to conclude that the ACTH-induced ultrastructural changes are the morphological expression of a stimulation of the cellular protein synthesis. Since mitochondria are largely autonomous in the synthesis of their enzymes and structural proteins, it is possible to hypothesize that ACTH also intervenes in the regulation of the mitochondrial protein synthesis.

Early Localization of 125I-Labeled Human Growth Hormone in Adrenals and Other Organs of Immature Hypophysectomized Rats

Abstract: Human growth hormone (HGH) labeled with 125I was injected intravenously into hypophysectomized, immature rats. One rat was frozen 6 min and another 20 min after injection by immersion in hexane cooled with dry ice. Whole-body sections were made of the frozen rats and autoradiograms were prepared by placing these sections on x-ray film. The autoradiograms revealed that, at both time intervals after injection, there was a high concentration of radioactive material in the kidney, liver and adrenal cortex. The only other tissues found to have a higher radioactive density than that of blood were the submandibular glands, nasal mucosa, gastric mucosa, bone and follicles of vibrissae. The radioactivity in the adrenal cortex was slightly higher in the zona glomerulosa than in the zona fasciculata and it was lowest in the zona reticularis. The concentration in the epiphyseal plates was no higher than that in bone or soft tissues. The radioactivity in the submandibular gland had the electrophoretic mobility of grow...

Assessment of adrenocortical function.

Abstract: OF the steroid hormones secreted by the human adrenal cortex into the adrenal venous effluent, only cortisol and aldosterone are essential to life processes. These steroids account for most of the ...

Congenital Adrenal Hyperplasia due to Deficiency of 11β-Hydroxylation of 17α-Hydroxylated Steroids1

Abstract: The case of an infant girl with congenital adrenal hyperplasia due to 11β-hydroxylase deficiency is described. The diagnosis was made at the age of 1 week and the steroid excretion of the untreated patient was followed during the first year of life. Urinary THS reached very high levels only after 16α-hydroxypregnenolone had disappeared from the urine, suggesting an influence of the physiologically reduced 3β-hydroxysteroid dehydrogenase activity of infancy on the steroid pattern induced by the 11β-hydroxylase deficiency. The secretion rate of S was extremely high and that of F was low normal, while the secretion rates of DOC and B and the aldosterone excretion were within normal limits. This indicates an impairment of the 11β-hydroxylation of 17α-hydroxylated compounds only and is indirect evidence for the existence of two 11β-hydroxylating systems in the human adrenal cortex.

Adrenocortical Atrophy and Diffuse Cerebral Sclerosis

Abstract: A boy, diagnosed as having Addison9s disease due to idiopathic atrophy of the adrenal glands at the age of 7 years, developed the first evidence of what was originally thought to be `Schilder9s disease9 at 8 years and 10 months. He died at 9 years and 11 months. There was a very striking family history of autoimmune disorders on the mother9s side. The clinical and pathological aspects of his case are outlined. Detailed studies of adrenal function during life showed a diminution in excretion of adrenal androgens and corticosteroids before therapy which was not evident from the 17-oxosteroid and 17-hydroxycorticosteroid assays in the resting state, though the initial diagnosis was based on the failure of ACTH to produce a rise in the 17-hydroxycorticosteroid excretion. No unusual or abnormal steroids were detected nor was there any disproportion between the androgen and corticosteroid excretion to suggest an adrenal enzyme deficiency. The biochemistry of the brain at necropsy revealed the changes expected in a demyelinating disorder, but the detection of abnormalities in the grey matter distinguished the condition from `Schilder9s disease9 in which the biochemistry of the grey matter is normal. There are 12 fully documented reports of boys with adrenocortical atrophy and diffuse cerebral sclerosis, and it is thought that this rare entity is inherited as an X-linked recessive characteristic. The two likely theories of causation involve either an error of metabolism common to the adrenal cortex and the brain, or the possibility that both the adrenal and brain pathology are due to an autoimmune disorder.

Catecholamine secretion by the adrenal medulla of the foetal and new-born foal.

Abstract: 1. The content and output of adrenaline and noradrenaline from the equine adrenal medulla has been investigated under different conditions in foetuses, foals and adult mares. 2. In the foetus only small amounts of both amines were secreted in response to stimulation of the peripheral ends of the splanchnic nerves to the gland; during anoxia the adrenal discharge was far greater and was independent of any nervous mechanism. 3. Whereas in the ruminant a direct adrenal response to low PO2 is confined to the noradrenaline cells during foetal life only, the adrenal medulla of the foetal foal secreted both adrenaline and noradrenaline during asphyxia, and the direct response persisted for some days after birth. Noradrenaline was the amine predominantly released during asphyxia in the foetus. 4. Catecholamine output from the equine adrenal medulla changed with age, in that there was a gradual increase in both the absolute and relative amount of adrenaline released, irrespective of the stimulus applied, although at any given stage of development a higher proportion of adrenaline was secreted in response to stimulation of the splanchnic nerves than during anoxia. 5. The relative proportions of the two amines in the effluent blood bore little resemblance to those found in the glands, removed after prolonged asphyxia, in either foetuses or foals. Preliminary observations have indicated that more noradrenaline is present in the glands when the foetus remains relatively undisturbed within the uterus. 6. The possible significance of the larger adrenal response to asphyxia in the foetal foal in comparison with other species is discussed in relation to the development of the innervation and the growth of the adrenal cortex.

Adrenocortical Control of Epinephrine Synthesis in Health and Disease

Abstract: Publisher Summary This chapter discusses adrenocortical control of epinephrine synthesis in health and disease. All species of vertebrates contain innervated cells that are derived from the neuroectoderm. However, only in mammals, chromaffin cells form a compact body, the adrenal medulla that takes on an envelope or cortex of steroid-secreting tissue during embryonic life. The cells of the adrenal cortex differ vastly from chromaffin cells: their embryonic anlage is not neuroectoderm but coelomic epithelium; they do not synthesize not water-soluble amines but lipid-soluble steriods and secrete them not in response to neuronal inputs but to a circulating hormone. The adrenal glands of mammals contain two distinct zones: (1) an outer cortex, which is homologous with the interrenal glands of lower vertebrates and which synthesizes glucocorticoid and mineralocorticoid hormones and (2) an inner medulla that is composed of chromaffin cells, which synthesizes norepinephrine and epinephrine. In certain species, these two zones are partially divided by an X-zone, which can secrete androgenic hormones. Otherwise, no capsule or sharp boundary separates the chromaffin cells from the steroid-producing cells.

The effect of ACTH on calcium distribution in the perfused cat adrenal gland.

Abstract: 1. Experiments were carried out to study the effects of adrenocorticotrophin (ACTH) on calcium distribution in the isolated cat adrenal gland perfused with Locke solution. 2. The addition of ACTH to Locke solution caused a small, but significant, increase in the radiocalcium (45Ca) space and content of the adrenal cortex. 3. The average 45Ca washout curve obtained after exposure to ACTH was significantly displaced above the average washout curve for the control glands during the first 20 min of washout. During the time that the two curves were significantly different, maximum corticosteroid secretion was attained. 4. The rate of 45Ca efflux was slowed after ACTH was added to the perfusion medium. 5. The total calcium content of the cortex was not altered by ACTH. 6. Perfusion with calcium-free Locke caused a rapid decrease in the calcium content of the cortex to about 20% of the control value. Dinitrophenol was required to deplete completely the cortical calcium content during perfusion with the calcium-deprived medium. 7. The results are consistent with the suggestion that a translocation of calcium occurs during stimulation of the cortex by ACTH. The source of the calcium ions needed to support the secretory response to ACTH is probably not the extracellular fluid; but ACTH may shift calcium from a rapidly exchanging to a more slowly exchanging cellular pool.

Mineral Element Correlation with Adenohypophyseal-Adrenal Cortex Function and Stress

Abstract: A statistical correlationl was made between adrenocorticotropin (ACTH) and four elements in rats under control, stress, and stress-recovery conditions. Blood serum zinc showed a strong positive correlation with the rise in ACTH during stress and its decline in stress recovery. Serum calcium, copper, and magnesium demonstrated little correlation with ACTH changes. The strong ACTH-zinc correlation points to an as yet undefined interaction between ACTH and zinc

Immobilization Stress Induced Changes in Adrenocortical and Medullary Cyclic AMP Content in the Rat

Abstract: The levels of adrenal cyclic AMP in adrenal cortex and medulla have been examined during immobilization stress under varying conditions. After 30 min of immobilization, there was a highly significant rise in whole adrenal cyclic AMP, returning to base line levels after 150 min. Theophylline pretreatment shifted the maximal cyclic AMP increase after immobilization to 10 min, with return to almost base line values at 30 min. Hypophysectomy blocked the rise in adrenal cyclic AMP and, in fact, there was a small but significant decrease after 10 or 30 min of immobilization. Denervation of the adrenal gland did not alter the level of cyclic AMP in unstressed animals but reduced the elevation of cyclic AMP to about 50% of the response observed in the intact adrenals of stressed animals. There was no increase in cyclic AMP in the adrenal medulla after stress although the medullary component of cyclic AMP was 50% of the total. There was a highly significant cortical increase in cyclic AMP after immobilization. Fin...

Possible Role of the Pituitary/Adrenocortical Axis in Aggressive Behaviour

Abstract: THE recent finding by Cherkin and Meinecke1 that aggressive behaviour in previously isolated male rabbits could be suppressed for some weeks by allowing them to recover in pairs from barbiturate anaesthesia, raises an interesting question concerning the action of components of the pituitary/adreno-cortical axis on behavioural responses. It is well established that most forms of anaesthesia are “stressful” in that they result in activation of the adrenal cortex, and the possibility thus exists that findings such as those by Gherkin and Meinecke are a consequence of changes in ACTH.

The fine structural morphology of adrenal cortices of normal and stressed squirrel monkeys.

Abstract: The fine structural morphology of the male squirrel monkey adrenal cortex has been examined When compared to other laboratory animals, the squirrel monkey adrenal cortex secretes large amounts of cortisol and maintains extraordinarily high plasma cortisol levels for prolonged periods of time The normal cortical cells have numerous mitochondria with either a tubulo-vesicular or lamellar internal membrane arrangement, a well-developed agranular endoplasmic reticulum which is arranged in juxtaposition to mitochondria and lipid droplets, several lysosomes, and numerous thin-walled blood vessels of large caliber, suggestive of a rich blood flow through the gland These characteristics have heretofore been associated with hypersecretion Their presence in the squirrel monkey cortex, known to have high secretory activity, lends credence to the correlation of hyperdevelopment of the agranular reticulum with increased rates of secretion of corticoids During chair restraint, the plasma cortisol levels rise two to three fold Adrenocortical cells thus stressed exhibit a depletion and disorientation of membranes both of the agranular endoplasmic reticulum and mitochondria and a loss of ribosomes, lysosomes and, to some degree, intracellular lipid The animal appears to be responding maximally to the stress of chair restraint These fine structural characteristics are interpreted as an example of an adrenal cortex in the process of becoming functionally exhausted, since these animals sometimes do not survive the stress of chair restraint

Effect of ACTH on mitochondrial RNA synthesis of rat adrenocortical cells

Abstract: The incorporation of 3H-thymidine and 3H-uridine into adrenocortical cells of intact and ACTH-treated rats was investigated by high-resolution autoradiography. The quantitative analysis of autoradiographs shows no effect of ACTH on the incorporation of 3H-thymidine, at least in our experimental conditions. On the contrary, ACTH was found to enhance the incorporation of 3H-uridine into both adrenocortical nuclei and mitochondria. These findings are discussed in relation to numerous biochemical and morphological data, indicating that ACTH stimulates the synthesis of enzymes and structural proteins of adrenocortical cells.

THE ISOLATION OF A RECEPTOR FOR ADENOSINE 3′,5′‐CYCLIC MONOPHOSPHATE (cAMP) FROM THE ADRENAL CORTEX: THE ROLE OF THE RECEPTOR IN THE MECHANISM OF ACTION OF cAMP*

Abstract: The function and growth of much of the adrenal cortex is controlled by adrenocorticotropic hormone ( ACTH) . Adrenal steroid hormone production is stimulated within minutes after the administration of ACTH. The injection of the hormone for several days or its secretion in excess as occurs in certain adrenal disease states causes an increase in the size and protein content of the gland. Following the removal of ACTH from the circulation, steroid hormone secretion .falls and the protein content of the adrenal cortex diminishes as the cells atrophy. The work of Sutherland's group indicated that the action of certain hormones is mediated by CAMP.' Haynes established that in the adrenal cortex ACTH causes an increase in the level of CAMP, and that the nucleotide substitutes for ACTH in inducing steroidogenesis.2. More recent investigations demonstrated that ACTH activates adenyl cyclase on the plasma membrane of the adrenal cell.4* The enzyme catalyzes the formation of cAMP and the nucleotide acts as the intracellular inducer of the action of ACTH. Inhibitors of protein synthesis were shown to block the stimulation of steroidogenesis by ACTH without affecting the activation of adenyl cyclase by the hormone.6-R Blocking RNA synthesis failed to prevent the induction of steroid hormone synthesis by ACTH.e-Q Therefore, it was postulated that ACTH acting through cAMP regulated adrenal function by modulating protein synthesis at the level of the translation of messenger RNA.10-12 Although these investigations suggested a hypothetical model for the action of cAMP in the adrenal cell, the mechanism by which the cyclic nucleotide regulated adrenal cell function remained unknown.

Perspectives in aldosterone and renin control.

Abstract: Summary: The factors which control sodium excretion by the kidney - the glomerular filtration rate, the action of the steroid hormones to increase tubular reabsorption of sodium, and other influences on tubular reabsorption, often grouped together under the general heading of “third factor”, e.g. proximal tubular salt losing hormone, oncotic pressure and vascular redistribution within the kidney - have been reviewed by Earley and Daugharty in 19691and Ehrlick in 19682. Aldosterone is the major mineralocorticoid of the adrenal gland and as such has an obvious ranking amongst those variables which can influence sodium metabolism. Aldosterone has another important relation with the kidney through the pressor peptide hormone angiotensin II which is one of the three factors known to be able to directly stimulate the zona glo-merulosa of the adrenal cortex to secrete aldosterone. Renin is a proteolytic enzyme released from the renal cortex which acts upon a specific globulin in plasma (renin substrate orangiotensino-gen) to produce the decapeptide angiotensin I. This in turn is converted into the hormone angiotensin II by the cleavage of a dipeptide from the C-terminal end. This conversion can be accomplished by “converting enzymes” which occur in blood or in the lungs. Angiotensin II is believed by some to be the most important variable in producing increased aldosterone secretion, especially during sodium restriction. Because this is believed to be the case, the factors which determine the angiotensin II level in blood could be more important than renin secretion per se, as this is only one sector of a complex system operating to increase arterial angiotensin II concentration.

Black adenoma of the human adrenal cortex

Abstract: A case of black adenoma of the human adrenal cortex is described in a 72‐year‐old man who died from renal failure due to analgesic nephropathy. This adenoma, which is of very rare occurrence, arises from the cells of the zona reticularis and/or interface cells between reticular and fasciculate zones. The black color is due to the very high population density of cytoplasmic granules of lysosomal nature. The evolutionary process from tiny intracortical nodule to larger adenoma is recorded and is analogous to that in the case of the much more common clear‐cell lesion.

The effects of cortisol and BUDR on cellular differentiation in the small intestine in suckling rats

Abstract: In suckling rats absorptive cells in the distal two-thirds of the small intestine ingest colloids by pinocytosis. In the middle third of the intestine pinocytosis ceases 17 to 21 days after birth and can be halted prematurely by glucocorticoids. The adrenal cortex is relatively inactive in newborn rats and begins to secrete glucocorticoids two weeks after birth; this secretion has been suspected to cause the termination of pinocytosis. Glucocorticoids do not stop pinocytosis in absorptive cells already present on the villi but induce the renewing population of cells in the crypts to replace the cells on the villi with new ones that do not engage in pinocytosis. Therefore, glucocorticoids act by inducing a new direction of cellular differentiation. BUDR (5-bromodeoxyuridine) is reported to inhibit cellular differentiation reversibly in vitro. When injected into 8 to 9-day-old rats, simultaneously with cortisol, it inhibited the change in cellular differentiation induced by cortisol; that is, pinocytosis continued unabated. BUDR did not appear to be toxic and did not interfere with cellular replacement in the small intestine, as judged autoradio-graphically. Thus it appears that BUDR inhibits the initiation of cellular differentiation by cortisol but does not interfere with cellular proliferation or the pre-established program of cellular differentiation that leads to pinocytosis. The mechanism of action of BUDR is still unknown; it is discussed in light of the possibility that BUDR may after cellular differentiation without acting directly on the genome.