Showing papers on "Adrenal cortex published in 1968"

Functions of the adrenal cortex

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Effect of Smoking and Nicotine on Adrenocortical Secretion

Abstract: The effect of tobacco smoking and nicotine administration on the secretory activity of the adrenal cortex was studied in man and in animals. In eight human subjects, there was a 27% to 77% rise in plasma 11-hydroxycorticosteroid (11-OHCS) concentrations after heavy cigarette smoking, compared to a normal diurnal fall during control observations with no smoking. In anesthetized dogs, nicotine administered intravenously resulted in a 64% rise in plasma corticosteroids. In rats, plasma corticosteroids concentrations increased 58% after intraperitoneal administration of nicotine, accompanied by an increase in the corticoid content of the adrenal glands and a decrease in their cholesterol content. It is suggested that this stimulation of adrenocortical activity is due to enhanced corticotropin release resulting from a nicotine-induced increase in sympathetic and catecholamine activity. Because of the physiological and pathological importance of adrenocortical hormones, their broad use as therapeutic agents, and their relationship to lipoprotein synthesis, the effect of cigarette smoking on adrenocortical secretion must be seriously regarded.

Immunological features of idiopathic Addison's disease: an antibody to cells producing steroid hormones

Abstract: Antibodies to adrenocortical cells, occurring in the serum of patients with idiopathic Addison's disease, were investigated by the indirect immunofluorescence technique. With selected human adrenal tissue obtained post mortem, staining was brightest in the innermost cells of the adrenal cortex. Strongly positive sera were observed to react with all thirty specimens of adrenal tissue examined, but lipid-depleted adrenocortical tissue provided the most suitable reagent for detecting weak antibody. Immunofluorescence tests upon twenty positive sera, using a wide range of human tissues, revealed in one serum an antibody, or antibodies, which reacted with all types of cells producing steroid hormones, namely testicular Leydig cells, hilus cells of the ovary and testis, theca interna and corpus luteal cells of the ovary, and placental trophoblast. A second, weaker example of `steroid-cell antibody' was detected among the twenty sera. The significance of steroid-cell antibody is discussed briefly in relation to steroid hormone biosynthesis and gonadal failure in idiopathic Addison's disease.

Site of Action of Trophic Hormones Upon the Biosynthetic Pathways to Steroid Hormones

Abstract: Slices of bovine adrenal cortex, bovine corpora lutea and rabbit testes were incubated with 20α-hydroxycholesterol-7α-3H or with cholesterol-7α-3H with and without the trophic hormones ACTH (adrenal cortex) or ICSH (corpora lutea or testes) added in vitro. In confirmation of previous findings, the trophic hormones increased the conversion of cholesterol-3H to cortisol-3H (adrenal cortex), progesterone-3H (corpora lutea) and testosterone-3H (testes). On the other hand, the trophic hormones produced a slight decrease in the conversion of 20α-hydroxycholesterol-3H to the same steroid hormones. In the case of the corpus luteum this decrease was less when incubation was continued for longer times, but under none of the conditions tested in any of the 3 tissues was the conversion of 20α-hydroxycholesterol-7α-3H to the steroid hormones increased in the presence of the trophic hormones. In the case of the testis similar results were observed 1 hr after a single intravenous injection of ICSH. These findings were m...

Incorporation of sulfate by the mouse thymus: its relation to secretion by medullary epithelial cells and to thymic lymphopoiesis.

Abstract: The thymus was examined in suckling mice during normal development and the involution and regeneration produced by injection of cortisol, in experiments designed to test the hypothesis that medullary epithelial cells secrete a ymphopoietic hormone responsible for controlling the magnitude of thymic lymphopoiesis. Cellular events were observed by light and electron microscopy. Lymphopoiesis was assessed, after injection of thymidine-3H, by counting the proportion of lymphocytes labeled in radioautographs of thymus. Cortical lymphopoiesis was distributed heterogeneously, being concentrated in the subcapsular region, but medullary lymphopoiesis was statistically homogeneous in distribution and similar in magnitude to the average level of cortical lymphopoiesis in suckling mice. Therefore counts of the labeling index in the medulla were used to estimate the size of the proliferating population of lymphocytes. Epithelial secretory activity was estimated by measuring the incorporation of 36sulfate by the thymus, using gel filtration chromatography to isolate soluble macromolecular 35sulfate—presumed on radioautographic evidence to represent the mucoid epithelial secretory product. Incorporated 35sulfate accumulated rapidly for 4 hr, reached a peak at 12 hr, and had fallen to half that level by 24 hr after a single injection—as would be expected of a secretory product. During normal postnatal development the size of the proliferating population of lymphocytes and the magnitude of 35sulfate incorporation increased in parallel. During acute involution induced by cortisol both parameters diminished greatly but rose to high levels during subsequent regeneration. Accordingly, lymphopoiesis and sulfate incorporation —as defined and measured in these experiments—correlated linearly over a wide range of variation, providing circumstantial evidence to support the hypothesis that medullary epithelial cells secrete a sulfated mucoid lymphopoietic hormone. This conclusion is discussed in terms of the roles of thymus and adrenal cortex in development of the lymphoid system and maturation of immunological competence.

Effects of actinomycin D and puromycin on the ACTH-induced ultrastructural transformation of mitochondria of cortical cells of rat adrenals in tissue culture.

Abstract: The ultrastructure of the mitochondria of the cultured cortical cells of rat adrenals was studied. In vivo it was found that the zona fasciculata mitochondria have vesicular internal structure. 600-A vesicles appear free in the matrix or as protrusions of the inner mitochondrial membrane. In tissue cultures of the fetal and newborn rat adrenal cortex it was seen that ACTH induces transformation of the tubulo-vesicular internal structure of the mitochondria to 600-A vesicles. Actinomycin D and puromycin inhibited this transformation if they were added with ACTH. When added alone, these inhibitors of protein synthesis induced no change in the ultrastructure of the mitochondria in cultured cortical cells of rat adrenals.

Control of Aldosterone Secretion

Abstract: Despite considerable controversy, the identities of the major mechanisms regulating aldosterone secretion are known and the broad outlines if not the details of how they operate are established. The release of this hormone from the zona glomerulosa of the adrenal cortex is increased by ACTH and by angiotensin II. The latter is formed in the blood stream by the action of renin from the kidney on a protein in the plasma. In addition to the hypothalamo-pituitary system and the renin-angiotensin system, a rise in plasma potassium or a fall in plasma sodium acts directly on the zona glomerulosa to increase aldosterone secretion. Additional stimulating and inhibiting factors from the posterior diencephalon and pineal gland may exist, but it now appears that, if they do, their physiological roles are minor.

Sensitivity to angiotensin and adrenocorticotrophic hormone in the sodium deficient rat.

Abstract: The effect of sodium deficiency, produced by 1 week of dietary salt restriction, on the adrenal response to angiotensin and adrenocorticotrophin (ACTH), singly and together, has been studied in acutely hypophysectomized-nephrectomized rats. Adrenal response was determined by the rate of secretion of aldosterone and corticosterone into adrenal vein blood as measured by the double isotope method. In sodium replete animals angiotensin did not significantly influence the secretion rate of either hormone. In sodium deficient animals it produced a significant increase in the secretion rate of aldosterone but not corticosterone. ACTH produced a significant increase in the secretion rates of both hormones. The response was similar in sodium replete and sodium deficient animals. When infused together in sodium replete animals the effect was no greater than with ACTH alone. However, when both hormones were infused together into sodium deficient animals the response in aldosterone secretion was even greater than the...

Inhibition of Adrenal Progesterone Biosynthesis by 3′,5′-Cyclic AMP

Abstract: 3′,5′-Cyclic AMP has been found to inhibit the transformation of pregnenolone to progesterone in rat adrenal homogenates. The inhibition of this transformation also takes place in microsome preparations and is reversed by NAD+. In mitochondria from beef adrenal cortex, which transform cholesterol-4-14C to pregnenolone, progesterone and more polar compounds, the presence of 3′,5′-cyclic AMP results in an accumulation of label in the pregnenolone pool with concomitant decrease in labeling of pools subsequent to pregnenolone. These effects of 3′,5′-cyclic AMP take place at concentrations higher than those reported to be present in adrenal tissue. (Endocrinology 82: 620, 1968)

Coexistence of primary ovarian insufficiency, primary adrenocortical insufficiency and idiopathic hypoparathyroidism.

Abstract: A patient is described who developed idiopathic hypoparathyroidism at age 3, primary ovarian failure at age 15, and primary adrenocortical failure at age 17. The primary nature of the ovarian insufficiency is indicated by the finding on several occasions of elevated urinary gonadotropin. The diagnosis of primary hypoadrenalism is based on absence of a rise in urinary 17-hydroxycorticoid excretion after 5 days of ACTH administration, and has been confirmed by the finding of elevated plasma ACTH. The combination of gonadal, adrenocortical and parathyroid failure has not been described previously. Antibodies to adrenal cortex, to thyroid antigens and to parietal cells of gastric mucosa have been demonstrated in the patient's plasma. It is postulated that the multiple glandular failure is the consequence of an auto-immune process.

Paradoxical Effects of the Androgen Antagonist Cyproterone Acetate on Steroid Metabolism in the Rat

Abstract: The androgen antagonist cyproterone acetate (Cyp Ac) was assayed for interaction with testosterone propionate (TP) in rats by using liver enzymes of cortisol metabolism, the adrenal cortex, the plasma cortisol binding globulin, the thymus and blood lymphocytes as target systems. In ovariectomized female rats as well as in neonatally castrated male rats, Cyp Ac given for 10 days at the age of 38 days or in adult life influenced the cortisol metabolism in liver homogenates in a way similar to that of TP. Both compounds strongly decreased the Δ4-3-keto reduction of cortisol to allotetrahydrocortisol and enhanced the formation of 3β- and 20β-hydroxy metabolites. However, when given in combination, Cyp Ac and TP significantly counteracted each other: in TP + Cyp Ac treated animals, on the one hand, the Δ4-3-keto reduction to allotetrahydrocortisol remained higher and the formation of 20β-hydroxy metabolites lower than in the animals treated with TP alone; on the other hand, the formation rate of 3β- and 20β-hy...

Asymptomatic production of ACTH. Radio immunoassay in squamous cell, oat cell and adenocarcinoma of the lung.

Abstract: Twenty-six patients with carcinoma of the lung and normal electrolytes were studied at the University of Texas M. D. Anderson Hospital. The most significant findings were: elevated plasma ACTH, lack of diurnal rhythm, and failure of dexamethasone to suppress plasma ACTH in eight patients. Two patients had oat cell carcinoma, three had squamous cell carcinoma and three had adenocarcinoma of the lung. ACTH-like material was found in the tumor tissue of one patient with squamous cell carcinoma. Plasma corticoids were elevated in 76% of the patients due to the effect of severe disease on the pituitary-adrenal axis and increased binding of plasma corticoids to plasma proteins. It is suggested that increased production of estrogen from the adrenal cortex may play an important role in the binding of cortisol to plasma protein. Plasma ACTH is the most reliable index in diagnosing “non-endocrine” Cushing's syndrome; it is an effective indicator of response to treatment or in determining the emergence of functioning metastasis.

Effect of ACTH on the electrical properties of adrenocortical cells.

Abstract: CELLS of the adrenal cortex have a membrane potential of −65 mV to −70 mV (ref. 1). No significant shift of this potential was apparent when steroidogenesis was stimulated by adrenocorticotrophin (ACTH) in normal Krebs–Henseleit medium2. In recent experiments with rabbit adrenal glands, using methods described previously1,2, we have observed that in medium free of K+, ACTH caused depolarization and often induced action potentials in adrenocortical cells.

Induction of epinephrine-forming enzyme by glucocorticoids: steroid hydroxylation and inductive effect.

Abstract: THE mammalian adrenal gland consists of two anatomically distinct regions; the inner medulla composed largely of catecholamine-producing chromaffin cells, and the outer cortex containing cells that secrete steroid hormones. Although these two adrenal components are derived from different primary germ layers, they come into close contact during embryonic life through an unusual process of tissue migration. Adrenaline is formed in the adrenal medulla through the N-methylation of noradrenaline1. This process is catalysed by an enzyme, phenylethanolamine-N-methyl transferase (PNMT), which is highly concentrated in adrenal chromaffin cells2 and also present in several areas of the brain3. PNMT activity is stimulated in the rat4–6 and the dog7 by hormones secreted from the anterior pituitary gland and the adrenal cortex.

Adrenocortical function related to methoxyflurane anaesthesia and surgery in man

Abstract: The effect of preanaesthetic medication, methoxyflurane anaesthesia, and surgery on free hydrocortisone (= 17-OHCS) concentrations in plasma were studied in eleven patients. The preanaesthetic medication significantly decreased plasma levels of free 17-OHCS, but the changes in concentration were variable after methoxyflurane anaesthesia for 30 minutes. Surgical stress evoked significant elevation of free 17-OHCS levels in plasma. These findings would imply that methoxyflurane anaesthesia is not a stressing agent for the adrenal cortex in man.

Steroid 3β-ol-Dehydrogenase Activity in the Cyclostome Gonad

Abstract: HISTOCHEMICAL techniques for the localization of the enzyme steroid 3β-ol-denydrogenase have been widely used to demonstrate the sites of cellular steroidogenesis. In mammals this enzyme has been demonstrated in the adrenal cortex, gonadal interstitium and placenta, and in non-mammalian species positive reactions have been observed in the somatic gonadal tissues of birds1,2, reptiles3, elasmobranchs4 and teleosts5–7. So far no studies of this kind seem to have been made on the gonads of the primitive agnathans.

A Finite State Model for the Control of Adrenal Cortical Steroid Secretion

Abstract: The steroid hormone Cortisol is the principal secretory product of the adrenal cortex in man and the carnivores. Its rate of secretion is primarily under the control of adrenocorticotropic hormone, or ACTH, secreted by the pituitary gland. The release of ACTH by the pituitary is in turn controlled by the hypothalamus by means of a neurohormone, corticotropin-releasing factor, or CRF. From the late 1940’s until early 1960’s there was a controversy about the mode of control of ACTH release and Cortisol secretion. One school based its view on the possibility of suppression of ACTH release and induction of adrenal atrophy by exogenous Cortisol, and suggested that there is closed-loop automatic control of the peripheral concentration of Cortisol in the blood, with stimulation of ACTH release when the Cortisol level of the blood fell, and suppression of that release when the Cortisol level was elevated. Accordingly, a stimulus would increase the load and lower Cortisol concentration. This would lead to increased CRF release from the hypothalamus and thus increased ACTH release from the pituitary.

The effect of sodium on renal renin and on glucose-6-phosphate dehydrogenase in the kidneys, salivary glands and adrenal glands. I. A histochemical and biochemical study.

Abstract: The effect of sodium balance upon renal renin and renal, adrenal, and salivary gland G-6-PD activity was studied quantitatively and histochemically in the rat. The results indicate a negative sodium balance (sodium deficient diet) induces marked increases in renal renin and G-6-PD content of the kidney and salivary gland. Histochemically, the changes in activity appeared throughout cortical nephrons, markedly so in the macula densa, in the excretory ducts of the salivary glands, and in the adrenal cortex, particularly the zona glomerulosa. Under positive sodium balance (high sodium diet), a marked reduction of G-6-PD activity was observed throughout; renal renin content was similarly reduced. The parallelism between stainable enzyme activity in the macula densa, juxtaglomerular granularity, and total renal G-6-PD and renin content suggests a functional interplay of the structures of the juxtaglomerular apparatus in response to sodium metabolism. Sodium balance also appears to affect enzyme activity of the adrenal cortex and salivary gland excretory ducts, either directly or through hormonal response.

Control of Corticotrophin Secretion

Abstract: It is now forty years since Smith (1927) showed that removal of the pituitary gland from various animal species results in atrophy of their adrenal cortices which can be prevented by the daily injection of anterior pituitary extracts or by transplants of adenohypophysial tissue. Thus, the existence of a trophic hormone responsible for the maintenance of the adrenal cortices was clearly shown. This hormone is called adrenocorticotrophic hormone, corticotrophin or ACTH. It is a comparatively simple polypeptide which varies slightly according to the species from which it is obtained. The chemical structures are known and some have been synthesised.

The Pharmacological Approach to the Study of the Mechanisms Regulating Acth Secretion

Abstract: The common association of sympathoadrenal and pituitary adrenocortical activity in stress has suggested that catecholamines play a special role in regulating ACTH secretion. Several theories have been proposed through the years to explain this relationship. These included (a) Long’s concept (1952) that emotional stimuli activate the hypothalamus which in turn stimulates the adrenal medulla via the spinal cord and splanchnic nerves, and the subsequently released epinephrine stimulates the release of ACTH; (b) Fortier et al.’s (1957) classification of emotional (epinephrine mediated) versus systemic stresses; (c) Smelik’s (1959) suggestion that “neurotropic” stresses result in the release of epinephrine from the adrenal medulla which would in turn activate “hypothalamic nervous pathways leading to the neurohypophysis; and (d) involvement of hypothalamic norepinephrine in the regulation of pituitary function (Vogt, 1954; Carlsson et al., 1962; Vernikos-Danellis, 1965). There is almost as much evidence for, as against any one of these theories and the vast number of reports in the literature using indiscriminately various psychodepressants and psychic energizers to “elucidate” the involvement of catecholamines in pituitary ACTH secretion have merely added to the confusion. This is brought out nicely in the review by De Wied (1967) on the effects of chlorpromazine on endocrine function.