Showing papers on "Corticosterone published in 1970"
TL;DR: Microscopic examination and consideration of steroid outputs suggest that preparations from decapsulated glands consist of zona fasciculata-reticularis cells, while those from capsular glands consist mainly of zzon glomerulosa cells with some zzon fascicULata contamination.
Abstract: Adrenal cells have been prepared, using crude collagenase, from the separated capsular and decapsulated portions of adrenals from intact rats. Microscopic examination and consideration of steroid outputs suggest that preparations from decapsulated glands consist of zona fasciculata-reticularis cells, while those from capsular glands consist mainly of zona glomerulosa cells with some zona fasciculata contamination. The yield of cells from the 2 preparations was of the order of 2 ×105 cells/adrenal for decapsulated glands and 1 ×lO5/adrenal for capsular glands. The endogenous output of 18-OH B, aldosterone, 18-OH DOC and corticosterone from the incubations of capsular and decapsulated gland cells has been examined. Three of the 4 steroids are produced by both types of cells; aldosterone production is virtually confined to capsular gland cells. The effect of ACTH, angiotensins, potassium and serotonin added in vitro on the output of corticosterone by decapsulated gland cells and that of corticosterone and al...
285 citations
TL;DR: Various steroids (1 7‐fl‐oestradiol, cortico‐sterone, deoxycorticosterone, progesterone, testosterone and androsterone) produced a dose‐dependent inhibition of the uptake of 3H‐noradrenaline by the Uptake2 mechanism in the isolated perfused heart.
Abstract: Various steroids (17-β-oestradiol, corticosterone, deoxycorticosterone, progesterone, testosterone and androsterone) produced a dose-dependent inhibition of the uptake of 3H-noradrenaline by the Uptake2 mechanism in the isolated perfused heart. It is suggested that these results may explain the potentiating effects of such steroids on the responses of vascular smooth muscle to catecholamines.
277 citations
TL;DR: The hypothesis that ACTH controls steroidogenesis by determining the rate of efflux of mitochondrial pregnanolone and hence the extent of the feedback inhibition by pregnenolone of its own synthesis is found to be consistent with the data obtained.
148 citations
TL;DR: The retention mechanism in hippocampal nuclei is highly specific for corticosterone and shows an interesting time dependence.
147 citations
114 citations
Journal Article•
101 citations
TL;DR: Evidence for the hypothesis that adrenal hormones may have a similar organizing effect on the developing central nervous system both with regard to neuroendocrine regulation of adrenocorticotropic hormone (ACTH) synthesis and release and with certain aspects of the behavior of adult organisms is discussed.
Abstract: Publisher Summary This chapter discusses evidence for the hypothesis that adrenal hormones may have a similar organizing effect on the developing central nervous system both with regard to neuroendocrine regulation of adrenocorticotropic hormone (ACTH) synthesis and release and with certain aspects of the behavior of adult organisms. An initial study discussed in the chapter reveals several interesting findings. The essence of these findings is that there is an extremely high level of adrenal activity in terms of both plasma and adrenal concentration of corticosterone in the newborn rat. There is also a clear and definitive response to administration of exogenous ACTH. However, following the initial period of high activity, there is a marked diminution of activity and the animal becomes unresponsive to ACTH and remains unresponsive until approximately 15 to 18 days of age. Pituitary ACTH increases markedly between 6 and 9 days of age. Adrenal corticosterone concentrations and plasma ACTH again appear at approximately 12 days of age, and by 15 days of age, the system appears to be totally active. In view of experimental data that were not compatible with the concept of an absolute stress non-responsive (SNR) period in the newborn, a series of investigations were undertaken to systematically investigate some of the parameters of the maturation of the organism's capacity to respond as indicated by significant changes in both plasma and adrenal corticoids, as well as in plasma and pituitary ACTH.
97 citations
TL;DR: The specific enzyme deficiency in various form? of congenital adrenal hyperplasia was elucidated and Metyrapone increased S and DOC secretion more than ACTH but decreased B, F and al...
Abstract: Using a previously described method for the simultaneous determination of the secretion rates of cortisol and aldosterone precursors, the specific enzyme deficiency in various form? of congenital adrenal hyperplasia was elucidated. Secretion rates of cortisol (F), 11-desoxycortisol (S), corticosterone (B), 11-desoxycorticosterone (DOC) and aldosterone (aldo) were determined in 10 normal subjects, 2 children with simple virilizing adrenal hyperplasia (21-hydroxylase defect) and 1 child with hypertensive virilizing adrenal hyperplasia (11-hydroxylase defect) under the following conditions: normal, low and high sodium (Na) diets, administration of metyrapone, dexamethasone and intravenous ACTH. The mean daily normal secretion rates were: F—7.5 mg/m2; S—0.26 mg/m2; B—2.2 mg/m2; DOC—0.055 mg/m2; aldo—0.13 mg/m2. Changes in dietary Na altered only aldo secretion. ACTH administration raised B and F secretion significantly. Metyrapone increased S and DOC secretion more than ACTH but decreased B, F and al...
74 citations
TL;DR: The circannual variation in circadian system phase of the adrenal cycle shown in this study cannot be regarded as an incomplete phase shift such as occurs shortly after an abrupt shift of the lighting regimen.
67 citations
64 citations
TL;DR: Aldosterone and corticosterone levels in cockerels were measured by the double isotope derivative assay in intact and surgically stressed animals as discussed by the authors, and the results indicated that the pituitary plays a role in maintaining the adrenal secretion of aldosterone.
TL;DR: PGE1 did not affect adrenal ascorbic acid in cortisol-pretreated intact rats or in 24-hr hypophysectomized rats, indicating that it has no ACTH-like effect on the adrenal cortex but acts by stimulating ACTH release.
Abstract: Prostaglandin E1 (PGE1) depleted adrenal ascorbic acid and cholesterol and increased plasma and adrenal corticosterone in rats. The log dose relationship between PGE1 iv and adrenal ascorbic acid concentration was linear between 0.5 and 2.0 μg. PGE1 was relatively specific since PGA1 and PGF2a did not deplete adrenal ascorbic acid at doses 10 times that of PGE1 and the respective vasopressor and vasodilator activities of the 3 prostaglandins did not correlate with capacity to stimulate the adrenal cortex. PGE1 did not affect adrenal ascorbic acid in cortisol-pretreated intact rats or in 24-hr hypophysectomized rats, indicating that it has no ACTH-like effect on the adrenal cortex but acts by stimulating ACTH release. Morphine strongly inhibited the adrenal ascorbic acid response to PGE1 in intact rats anesthetized with pentobarbital, indicating that the action of PGE1 on ACTH release is not direct on the anterior pituitary gland but is at some level in the central nervous system, possibly the hypothalamus...
TL;DR: Dose response curves for adrenals (H) showed that higher concentrations of continuously infused ACH increased corticosterone output rate 13-fold within 1 hr almost to that of Adrenals (I) similarly infused, which were not attributable to irreversible changes in the tissue during superfusion.
Abstract: Decapsulated rat adrenals were continuously superfused and corticosterone outputs assayed by competitive protein binding or soda fluorescence. During 5 hr superfusions, corticosterone output rate of adrenals (H) from acutely hypophysectomized rats remained almost constant (0.3–0.5 μg/rat/hr), whereas that of adrenals (I) from intact rats declined rapidly from high initial values (7 μgxylrat/hr) and approached that of adrenals (H). Release of preformed steroid could not explain this decline, which is ascribed to the decaying in vivo ACTH stimulus. Continuous ACTH infusion (64 mU/ ml) to adrenals (H) increased corticosterone output rate 13-fold within 1 hr almost to that of adrenals (I) similarly infused. After 2 hr the output rates of adrenals (H and I) each continuously infused with ACTH showed similar substantial declines, which were not attributable to irreversible changes in the tissue during superfusion. Dose response curves for adrenals (H) showed that higher concentrations of continuously infused AC...
TL;DR: Evidence is presented that hormone within brain cell nuclei is bound to a macromolecular component, probably protein, which can be extracted from isolated nuclei by 0.4 M NaCl.
Abstract: CORTICOSTERONE, the principal adrenal steroid in the rat,, is retained by cell nuclei in the brain of adrenalectomized rats by a process specific to the corticosterone structure1. Nuclear binding of hormone is greatest in the hippocampus, where we have previously found the highest tissue concentration of radioactive hormone, but is also significant throughout the rest of the brain1,2. The binding of steroid hormone to cell nuclei in other target tissues, indicates that the hormone receptor is protein which can be extracted from the nuclei by moderate salt concentrations3–6. We now present evidence that hormone within brain cell nuclei is bound to a macromolecular component, probably protein, which can be extracted from isolated nuclei by 0.4 M NaCl.
TL;DR: Gonadotropin neither induced relapse nor potentiated the induction of relapse by corticosterone, casting doubt on the hypothesis that spring relapse in malarial infections is mediated by seasonal changes in reproductive hormone levels.
Abstract: Previous work demonstrated that corticosterone induces relapse of avian malaria, and that this effect varies markedly from winter to spring. In the present study, English sparrows with latent Plasmodium relictum infections were treated in winter with corticosterone, gonadotropin, corticosterone + gonadotropin, or a control regimen consisting of the oil vehicle. Gonadotropin neither induced relapse nor potentiated the induction of relapse by corticosterone. These data cast doubt on the hypothesis that spring relapse in malarial infections is mediated by seasonal changes in reproductive hormone levels.
TL;DR: Comparison of outputs from bisected whole glands, capsular and decapsulated tissue has shown that 3 of the 4 steroids examined were produced to some extent by both zones of the adrenal cortex but aldosterone production was restricted to the zona glomerulosa under all conditions studied.
Abstract: Steroid output from adrenals of normal intact rats and rats 3 hr and 2 days after hypophysectomy has been measured during continuous superfusion in vitro (1, 2). Comparison of outputs from bisected whole glands, capsular (fibrous capsule plus mainly zona glomerulosa) and decapsulated (mainly zona fasciculata-reticularis plus medulla) tissue has shown that 3 of the 4 steroids examined, 18-hydroxy-β4, 18-hydroxy-DOC and corticosterone, were produced to some extent by both zones of the adrenal cortex but aldosterone production was restricted to the zona glomerulosa under all conditions studied. A reproducible decline in steroid output with time of superfusion was observed for all 3 types of tissue taken from normal intact rats. Three and 48 hr after hypophysectomy the production of the 3 steroids by the zona fasciculata was lowered and the decay virtually abolished. A continuous infusion of ACTH (60 mU/ml medium) maintained steroid output from the zona fasciculata of intact rats at the high initial level for...
TL;DR: Plasma levels of cortisol and corticosterone were determined in 18 lactating, nonpregnant dairy cows of three breeds and also at hourly intervals following a single injection of 200 IU ACTH to five cows and no treatment to one cow.
TL;DR: Results indicate a zone specificity of certain stimulators and confirm that they act at an early stage in the corticosteroid biosynthetic pathway preceding the formation of deoxycorticosterone.
Abstract: Capsular and decapsulated adrenal glands of rats kept on different diets were separately incubated with and without stimulators of aldosterone biosynthesis. The steroidogenic effect of serotonin, potassium ions and angiotensin II was limited to the capsular portion (zona glomerulosa), whereas ACTH and cyclic AMP acted on both the capsular and the decapsulated portion (zona fasciculata-reticularis) of the adrenal cortex. In capsular adrenal glands of normal and sodium-deficient rats all these agents stimulated aldosterone production severalfold and had a smaller effect on corticosterone output. Sodium deficiency led to a decreased response in corticosterone and deoxycorticosterone output. In capsular glands of potassium-deficient rats the stimulators did not enhance aldosterone production but actsd mainly on deoxycorticosterone output. ACTH enhanced corticosteron e and deoxycorticosterone output to a similar extent in decapsulated glands of all groups of experimental animals. These results indicate a zone specificity of certain stimulators and confirm that they act at an early stage in the corticosteroid biosynthetic pathway preceding the formation of deoxycorticosterone. On the other hand, changes in sodium and potassium balance induce alterations in the activity of the enzymes involved in the conversion of deoxycorticosterone to aldosterone and thus influence the steroidogenic response of the zona glomerulosa to stimulating agents.
TL;DR: The effect of ACTH upon the inhibition of corticosteroidogenesis produced by treating rats with several synthetic adrogens and treatment of rats with all 3 androgens brought about the decrease in cytochrome P-450 levels, whereas when metyrapone, a nonsteroidal competitive inhibitor of steroid 11β-hydroxylase, was given to rats for 6 weeks no change occurred.
Abstract: The effect of ACTH upon the inhibition of corticosteroidogenesis produced by treating rats with several synthetic adrogens has been evaluated. In experiments lasting about 2 weeks in which the simultaneous treatment with ACTH prevented the fall in adrenal weight due to the androgen therapy, corticosteroidogenesis measured in adrenal homogenates was still greatly reduced. Associated with the reduced production of corticosterone from progesterone there was a marked fall in the level of adrenal mitochondrial cytochrome P-450. The fall in cytochrome P-450 was not prevented by simultaneous treatment with ACTH. Treatment of rats with all 3 androgens, 17α-methylandrostenediol, 17α-methyltestosterone and 11β-hydroxy- 17α-methyltestosterone, brought about the decrease in cytochrome P-450 levels, whereas when metyrapone, a nonsteroidal competitive inhibitor of steroid 11β-hydroxylase, was given to rats for 6 weeks no change occurred in the level of adrenal mitochondrial cytochrome P-450. These data suggest that thi...
TL;DR: In sodium-depleted rats an intact pituitary was found to be essential for normal stimulation and maintenance of aldosterone production, and the ability of pituitsary hormones to maintain the elevated ald testosterone secretion and in vitro production rate was studied.
Abstract: In sodium-depleted rats an intact pituitary was found to be essential for normal stimulation and maintenance of aldosterone production. To define better this pituitary involvement the effects on aldosterone production of whole and posterior pituitary extracts, ACTH, GH, FSH, LH and l-thyroxin injections were studied in hypophysectomized rats fed a diet low in sodium. None of the injections resulted in aldosterone secretion rates which approached those measured in intact, sodium-depleted rats. Whole pituitary extracts, ACTH and GH had some aldosterone stimulatory effect. In order to avoid the effects of prolonged hypophysectomy, rats were first sodium depleted and then hypophysectomized. The ability of pituitary hormones to maintain the elevated aldosterone secretion and in vitro production rate was studied. ACTH only partially maintained aldosterone secretion and in vitro production while maintaining corticosterone production in vitro. GH also partially maintained aldosterone secretion and production but ...
TL;DR: The effects of prepuberal gonadectomy on adrenal function were studied in both male and female rats and Corticosterone added in vitro to adrenal tissue from gonadectomized rats was converted to a fluorescence negative, ultraviolet negative, blue tetrazolium positive metabolite.
Abstract: The effects of prepuberal gonadectomy on adrenal function were studied in both male and female rats. Steroid production was measured in vitro using either adrenal homogenates or slices. Adrenal tissue from castrated animals of either sex produced less steroid when determined by acid fluorescence or ultraviolet absorption. The effect was reversed after replacement with testosterone or estradiol. No difference due to castration was observed when steroid production was measured with blue tetrazolium. Corticosterone added in vitro to adrenal tissue from gonadectomized rats was converted to a fluorescence negative, ultraviolet negative, blue tetrazolium positive metabolite. This conversion was inhibited by gonadal hormone replacement in vivo. The metabolite was identified by Rf both before and after acetylation on several paper and thin layer chromatographic systems and also by infrared spectroscopy as 3β,5α-tetrahydrocorticosterone (compound R). Two additional compounds tentatively identified by chromatograph...
TL;DR: The distribution of glucocorticoids observed in the Amphibia and a possible cause of corticosterone response to dehydration was discussed.
TL;DR: The most important morphological parameter for assessing the activity of a steroid-secreting cell is the quantity of smooth endoplasmic reticulum, and it is possible to hypothesize that ACTH intervenes in the regulation of the mitochondrial RNA and DNA synthesis.
Abstract: The effects of corticosterone on adrenocortical cells of intact and hypophysectomized ACTH-treated rats were investigated by morphometric and autoradiographic methods The data obtained in these experiments allow us to make the following conclusions:
TL;DR: A general conceptual framework within which behavioral effects of corticosterone can be recognized and studied is discussed, which indicates that adrenal steroids act directly on the brain to regulate release of ACTH from the pituitary and to moderate neural activity underlying behavioral responses.
Abstract: Publisher Summary This chapter discusses a general conceptual framework within which behavioral effects of corticosterone can be recognized and studied The primary requirement for the brain to act as a sensing device for the regulation of adrenocorticotropic hormone (ACTH) secretion and as a target organ for corticosterone to influence neural activity and behavior is that the hormone be able to enter the brain in increasing amounts as the blood level increases, as it does in stress This chapter focuses on the physiological and behavioral consequences of corticosterone action on the hippocampus and other regions of the brain There is a growing body of evidence that indicates that adrenal steroids act directly on the brain to regulate release of ACTH from the pituitary and to moderate neural activity underlying behavioral responses Lesion and electrical stimulation studies of the limbic system indicate that the hippocampus, as part of a delicately counterbalanced system of excitation and inhibition converging on the median eminence (ME), has an inhibitory influence on ACTH release
TL;DR: Analysis of tissular radioactivity and steroid metabolism showed that steroid incorporation (greater for progesterone) and steroid catabolism (faster for cortisol) were responsible of these binding differences.
TL;DR: Investigation of plasma and adrenal corticosterone levels in male rats indicates that different pathways or mechanisms are involved in the stimulation of adrenocortical activity which is a response common to several different toxic chemicals and other stresses.
TL;DR: It is concluded that corticosterone, the circulating adrenal glucocorticoid of the rat, will, in physiological concentrations, act directly on the cells of the adenohypophysis to decrease their responsivity to CRF activity, which will allow variation in the rate of secretion of ACTH even with a constant rate of glandular secretion of CRF.
Abstract: The addition of corticosterone (1 µg/ml) to rat adenohypophyses incubated in KRB depressed spontaneous ACTH release and suppressed the augmented release of ACTH induced by a crude acid extract of rat hypothalamus stalk-median eminence (HSME). Concentrations of corticosterone within the physiological range (0.50 and 0.25 µg/ml) did not depress spontaneous release, but did suppress the HSMEinduced release of ACTH. We conclude that corticosterone, the circulating adrenal glucocorticoid of the rat, will, in physiological concentrations, act directly on the cells of the adenohypophysis to decrease their responsivity to CRF activity. This will allow variation in the rate of secretion of ACTH even with a constant rate of secretion of CRF. (Endocrinology 87: 371, 1970)