Showing papers on "Adrenal cortex published in 1972"

Studies of the control of plasma aldosterone concentration in normal man: II. Effect of dietary potassium and acute potassium infusion

Abstract: The responses of plasma aldosterone, cortisol, and corticosterone to an infusion of 75 mEq of potassium chloride over 120 min were studied in 10 normal subjects. Five subjects were fed a 10 mEq and five a 200 mEq sodium diet, while all subjects ingested 40 mEq and 200 mEq potassium sequentially. Two potassium infusions were performed in each subject when in balance on a fixed sodium intake and low and then high potassium diets. Regardless of dietary intake, increases of serum potassium of 0.5-1.5 mEq/liter above preinfusion levels were usually associated with significant increments in plasma aldosterone concentration. Our data agree with previous evidence that the potassium ion stimulates the adrenal cortex directly to secrete aldosterone. Peripheral renin activity did not increase after the potassium infusion. Plasma cortisol and corticosterone levels generally followed the expected diurnal decline during the infusion, implying that ACTH secretion did not increase. The plasma aldosterone response to incremental changes in serum potassium was linear on each of the four diets. The slopes of these linear relationships increased significantly when the potassium intake was increased from 40 to 200 mEq. No increase in slope occurred on either potassium intake when dietary sodium was restricted from 200 to 10 mEq. Thus, identical increases in serum potassium were associated with greater increments in plasma aldosterone above preinfusion levels on either sodium intake when the 200 mEq potassium diet was compared with the 40 mEq potassium intake.

Adrenocortical Control of the Biosynthesis of Epinephrine and Proteins in the Adrenal Medulla

Abstract: The activity of phenylethanolamine-N-methyl transferase (PNMT) in the adrenal medulla declines markedly after hypophysectomy. Enzyme activity is restored if animals are treated with ACTH or very large doses of glucocorticoids, but not by "replacement" doses of glucocorticoids or by other pituitary or adrenal hormones. These observations indicate that basal levels of PNMT activity require that the medulla receive the very high concentrations of hydrocortisone or corticosterone that are available to it by virtue of its unique location within an envelope of adrenal cortex. The resotration by dexamethasone treatment of the PNMT activity in medullas of hypophysectomized animals is blocked by concurrent administration of actinomycin D or puromycin. Moreover, hypophysectomy is associated with decreases in the quantity of immunochemically assayable PNMT protein in the medulla and in the rate at which PNMT is synthesized from isotopically labeled amino acid precursors. These changes are also reversed by dexamethasone. Adrenomedullary polysomes are markedly disaggregated after hypophysectomy; however, polysome patterns revert to normal if animals are treated with ACTH or dexamethasone. These observations all suggest that glucocorticoids stimulate the synthesis not only of PNMT, but also of a wide variety of medullary proteins. The decrease in adrenal PNMT activity caused by hypophysectomy is associated with corresponding decreases in the mass of chromaffin cells and in the amounts of epinephrine stored in the adrenal medulla and secreted in response to physiological stimuli. After the induction of insulin hypoglycemia, adrenals of hypophysectomized dogs release considerably less epinephrine, and more norepinephrine, than those of control animals. Inasmuch as norepinephrine is far less potent than epinephrine in accelerating the breakdown of glycogen, the impairment in epinephrine synthesis caused by pituitary insufficiency may be related to the insulin sensitivity that often characterizes this disease.

Alterations of adrenal cortex and thyroid in mice with congenital absence of the thymus.

Abstract: THE possible role of endocrine factors in the thymus and their control by hormones of the adenohypophysis or its target glands has been investigated extensively in animal models. These include mice whose pituitary function has been inhibited or blocked by anti-pituitary serum1–3 or anti-growth-hormone serum4–6, neonatally thymectomized mice1,3,7–9, and the genetically hypopituitary dwarf mice with thymus atrophy10–12. Further opportunities have been offered by the observation that genetically hairless “nude” mice (genetic symbol: nu)13 have no thymus14,15.

Mechanism of ACTH action

Abstract: ACTH regulates both the differentiated function (steroidogenesis) and the growth and replicative potential of the adrenal cortex. Cyclic AMP (cAMP) serves as the mediator of ACTH action within the cell. The binding of cAMP to its specific receptor activates a protein phosphokinase enzyme with resultant phosphorylation and altered function of several important substrates. The regulation of steroidogenesis requires protein synthesis and affects the conversion of cholesterol to pregnenolone, the rate-limiting step under hormonal control. In normal adrenal cortical tissue, ACTH stimulates DNA synthesis and replication, and in a functional adrenal tumor in tissue culture, ACTH inhibits DNA synthesis and replication. ACTH and cAMP thus appear to direct the adrenal cell toward the differentiated, maximally functional state.

Chronic and acute dexamethasone suppression of stress activation of the adrenal cortex in young and aged rats.

Abstract: Adrenocortical responsiveness to ether vapor stress was measured in young adult (4–6 months) and aged (22–32 months) rats subjected to acute and chronic treatments with dexamethasone. Daily administra

The endocrine response to trauma

Abstract: Publisher Summary An increased production of hormones after injury is part of a basic defense mechanism for survival, and absence or failure of some glands, such as the adrenal cortex, is associated with the circulatory collapse after injury. Several investigations involving standard infusions of cortisol to patients before and immediately after surgery indicate that the rate of disappearance of 17-hydroxycorticosteroids is reduced by stress, and that the impaired hepatic removal of free 17-hydroxycorticosteroids is an important factor in maintaining the raised plasma levels immediately after surgery. The responsiveness of the adrenal cortex to stress is related to blood flow through the gland. Patients in severe shock are found to have very low plasma cortisol levels, which rise sharply after successful resuscitation. The regulation of adrenocorticotropic hormone (ACTH) secretion during stress is outside the control of the normal negative feedback mechanism. This mechanism persists during stress but the control point is raised.

Schilder's Disease: Sex-Linked Recessive Transmission With Specific Adrenal Changes

Abstract: The adrenal glands from ten patients with Schilder's disease, of whom four were familial and nine were male, were examined. Many cells of the zona reticularis and fasciculata were ballooned and often contained crystalline aggregates. The X-linked recessive inheritance and this derangement of the adrenal cortex in males with Schilder's disease strongly indicate the presence of a metabolic process.

Identification of peroxisomes in the rat adrenal cortex.

Abstract: Organelles with the ultrastructure and cytochemical characteristics of peroxisomes (microbodies) have been identified in cells of the zona fasciculata and zona reticularis of the rat adrenal cortex. These peroxisomes appear as small, elliptical to spherical or branched structures, enclosed by a single membrane and composed of a moderately electron-dense matrix. They do not possess a nucleoid or core of the type found in peroxisomes of liver and kidney. These organelles show a strongly positive staining reaction with the diaminobenzidine technique for peroxidatic activity of catalase. This staining is inhibited by aminotriazole. In cytochemical preparations revealing acid phosphatase activity, lysosomes are strongly stained and peroxisomes are free of reaction product.

A comparative ultrastructural study of the effects of chlorphentermine and triparanol in rat lung and adrenal gland

Abstract: Chlorphentermine, an anorectic drug, and triparanol, an inhibitor of cholesterol biosynthesis, induce cytological alterations of essentially identical ultrastructural patterns, in pulmonary tissue and in adrenal cortex and medulla of the rat. In lung tissue, the predominant features are 1) the occurrence of numerous concentric lamellar inclusion bodies in alveolar macrophages, the number and size of which become increased, 2) the occurrence of lamellar inclusions as well as 3) unit-membrane-limited, dense cytoplasmic bodies, having a reticular or a crystalloid structure, in nearly all sessile cell types of pulmonary tissue. Pleomorphic inclusion bodies of the same kind occur in increased numbers within the cells of adrenal cortex and medulla. Irrespectively of the drug and of the type of cell, most lamellar bodies display a periodicity of approximately 45 A, suggesting phospholipids or other lipids to be the major constituents of the inclusions. The observed cytological modifications are believed to reflect an abnormal intracellular accumulation of lipids.

The effect of serotonin and potassium on corticosterone and aldosterone production by isolated zona glomerulosa cells of the rat adrenal cortex.

Abstract: THE EFFECT OF SEROTONIN AND POTASSIUM ON CORTICOSTERONE AND ALDOSTERONE PRODUCTION BY ISOLATED ZONA GLOMERULOSA CELLS OF THE RAT ADRENAL CORTEX

Secretion of ACTH and β-MSH by an Adrenal Medullary Paraganglioma

Abstract: A 41-yr-old woman with Cushing's syndrome was shown to have a right adrenal medullary tumor and bilateral adrenocortical hyperplasia by adrenal venography. Her cortisolism was very marked and was unaffected by administration of ACTH, metyrapone, or dexamethasone. She had elevated plasma ACTH and β-MSH without an apparent normal circadian rhythm. Plasma samples obtained by selective venous catheterization suggested that the tumor was the source of ACTH and β-MSH and that the hyperplastic adrenal cortex was the source of cortisol. The tumor was found on postmortem examination to be a non-chromafnn paraganglioma which contained immunoreactive ACTH. Clinical and biochemical evidence of catecholamine excess was absent.

Plasma Corticotropin, Cortisol and Growth Hormone Responses to Hypoglycemia in the Morning and Evening

Abstract: Plasma corticotropin (ACTH), growth hormone (GH) and cortisol responses to the iv injection of insulin at 9 am and 9pm were studied in normal subjects. ACTH and GH were determined by radioimmunoassay and cortisol by fluorometry. There were no significant differences between the absolute values of plasma ACTH, GH or cortisol concentrations observed following insulin hypoglycemia induced in the morning and in the evening, while the increment of plasma cortisol concentration from the basal level in the 9pm experiment was significantly higher than that of the 9 am experiment at 45, 60 and 90 min after insulin injection. The apparent discrepancy between the increment of cortisol concentration and ACTH concentration in plasma was discussed in relation to the normal response characteristics of the adrenal cortex to ACTH.

A new crystal-containing cell in human adrenal cortex.

Abstract: Electron microscope examination of the adrenal cortex from three male human subjects revealed a special type of cell occurring in periendothelial spaces, in all adrenal cortex zones. It is a clear, spindle-shaped cell the principal cytoplasmic features of which are crystalline inclusions with a structure similar to that of the Reinke crystals of human testicular interstitial cells and an abundance of microfilaments. Enzymatic digestions with pronase, pepsin, and ribonuclease were performed, and no digestion of the crystals was obtained. The crystals had no peroxidase or acid phosphatase activities. This cell appears to be exclusive to human males and it may be related to adrenal androgen secretion.

On the fine structure of alteration of the adrenal cortex in hypophysectomized rats.

Abstract: The adrenal cortex of normal and hypophysectomized rats was observed by electron microscopy 5–90 days after the operation and, chiefly, the degeneration mechanism of the cortical tissue was discussed. In normal rats mitochondrial inner structures are generally tubular in shape in glomerulosa cells, vesicular (and tubulo-vesicular) in fasciculate cells and tubulo-vesicular (and vesicular) in reticularis cells. Some mitochondria in a few glomerulosa cells show long straight tubular crests in normal as well as hypophysectomized rats. Usually lipid droplets in normal glomerulosa, fasciculate and reticularis cells are surrounded by elements of smooth endoplasmic reticulum, which are very closely associated with mitochondria. About 10–25 days after hypophysectomy, most mitochondria in fasciculate and reticularis cells show tubular crests, and numerous electron lucent lipid droplets are accumulated in these cells. These droplets occupy most parts of the cytoplasm and are sometimes in contact with one another or with mitochondria. The elements of smooth endoplasmic reticulum and Golgi apparatus are markedly reduced in number and size. About 10–90 days after the hypophysectomy, the degenerative cortical cells containing irregularly shaped nuclei, heterogeneously dense bodies in various sizes, and a large number of electron lucent lipid droplets are seen. The author speculates that most fasciculate and reticularis cells degenerate because of a disorder in the lipid metabolism, since ACTH release, which is necessary for synthesis of corticosteroid hormones from cholesterol, is absent in hypophysectomy. The fatty degeneration of the fasciculate and reticularis cells is considered to be a main cause for attenuation of the cortical tissue. Sometimes atrophied cortical cells without lipid droplets are also found 60–90 days after hypophysectomy.

Role of calcium and adenosine cyclic 3'-5' phosphate in action of adrenocorticotropin.

Abstract: ALTHOUGH adenosine cyclic monophosphate (cyclic AMP) has been proposed as a mediator through which many hormones exert their physiological effects1, it is also well established that calcium plays a crucial role in hormone release2. Both calcium3,4 and cyclic AMP1,5 have been implicated in the action of adrenocorticotropin (ACTH) on the adrenal cortex and although various hypotheses have been advanced concerning their roles in steroid production and release, elucidation of their functions in the adrenal gland is hindered because most studies have been carried out on in vitro systems where the physiological release response cannot be studied. The isolated cat adrenal gland perfused in situ 6 approximates the situation in vivo, yet eliminates the influence of several factors, including the anterior pituitary. In the intact adrenal preparation one can also measure both steroid synthesis and release and can better evaluate the respective effects of cyclic AMP and calcium on these processes.

Low renin hypertension and the adrenal cortex.

Abstract: THE concept that the adrenal cortex might be involved in the development of hypertension has been speculated upon by endocrinologists for approximately 60 years. In the early 1900's, Achard and Thiers1 described a patient with hypertension and marked hirsutism who at autopsy was found to have bilaterally enlarged adrenal glands. They implied that the hypertension and the hirsutism were due to some abnormality within the adrenal glands. This concept lay dormant for about 20 years, until Cushing2 reported the syndrome that is now named after him. Hypertension was a prominent part of this syndrome, and the implication was that the . . .

Tissue culture of rat adult decapsulated adrenal glands. A methodological, ultrastructural and morphometric investigation.

Abstract: A method of cultivation involving both repeated trypsinisations (at room temperature) and explantation of the tissue fragments on polythene discs has been shown to be apt to the growth in vitro of rat adult decapsulated adreno-cortical tissue. This is the first time that the successful cultivation of such a tissue is reported. The technique and its applications are discussed. The effects of β1–24 corticotrophin (ACTH1–24) on the rat adult adrenal cultures have been examined by both electron microscopy and autoradiography. Zona fasciculata and reticularis cells grown in the absence of ACTH for long terms (15–16 days) survive and proliferate as dedifferentiated elements. If ACTH1–24 is added to the cultures, adrenocortical cells will, within 2 days, simultaneously increase their proliferation rate and differentiate. After 7 days of treatment, cortical cells exhibit not only fully differentiated but even hypertrophic morphologic features. Significant stimulations of adrenal DNA, RNA and gross protein synthesis have been found to take place at different times after the starting of the ACTH1–24 treatment. These data are discussed in relation to the findings previously reported in literature. Rat adult adrenal gland tissue cultures are proposed as a non-previously available tool for investigations into the physiopathology of the adrenal cells to be carried out in a carefully controlled environment.

Carcinoma of the adrenal cortex with hyperaldosteronism.

Abstract: A 34-year-old woman with hypertension and hypokalemia was found to have a carcinoma of the adrenal cortex. Excretion of urinary corticoids and 17-ketosteroids was normal. Urinary aldosterone excretion was high and was unchanged by sodium loading and plasma renin concentration was low. She has remained well for 6 months following surgery with return of blood pressure and serum potassium to normal.