Adrenocortical Secretion Research Articles

A Relationship between Brain Serotonin and Adrenocortical Secretion and its Possible Significance in Endogenous Depression*

There is evidence for disturbances of 5-hydroxytryptamine metabolism and of the pituitaryadrenal system in depression. Animal experiments indicate that these disturbances may be metabolically related through the enzyme tryptophan pyrrolase, synthesis of which depends upon adrenal activity. The possible significances of these changes in the development of depressive illness and their therapeutic implications are discussed. * Die Arbeit wurde mit einem Preis der Anna-Monika-Stiftung ausgezeichnet. Storungen des 5-Hydroxytryptaminstoffwechsels und des Hypophysennebennierenrindensystems bei der Depression sind beweisbar. Tierversuche lassen die Deutung zu, das diese Storungen im Stoffwechsel durch das Enzym Tryptophanpyrrolase bedingt werden, dessen Synthese von der Aktivitat der Nebennierenrinde abhangt. Die mogliche Bedeutung dieser Veranderungen fur die Entwicklung depressiver Erkrankungen und ihre therapeutischen Folgerungen werden diskutiert.

Phosphoserine phosphatase: Development formation and hormonal regulation in rat tissues

Phosphoserine phosphatase was measured in rat liver and kidney as a function of age, sex, and treatment with different endocrine or metabolic factors. Several differences were found between liver and kidney in the regulation of this enzyme. The phosphoserine phosphatase activity of adult liver was 595 units per g for males, 383 for females, and for adult kidney of both sexes it was 1266. Estrogen treatment raised the level of phosphoserine phosphatase in kidneys after the age of 25 days but not in livers. The high levels of phosphoserine phosphatase in fetal liver, 2500 units per g, decreased to 900 during the last 4 days of gestation and the first 3 postnatal days. During the same time period kidney phosphoserine phosphatase increased from insignificant levels to about 600 units per g. The administration of hydrocortisone (but not of thyroxine, glucagon, or serine) to fetal rats enhanced the decline of liver phosphoserine phosphatase, suggesting that adrenocortical secretion is the stimulus for the normal decrease in liver phosphoserine phosphatase during late fetal life. The injection of hydrocortisone to the pregnant rat also resulted in lower phosphoserine phosphatase in the livers of her fetuses or newborns.

Stimulation of adrenocortical secretion by nicotinic acid and certain of its derivatives and analogues

The effect of nicotinic acid, nicotinamide, and related substances on adrenocortical secretion has been investigated. Nicotinic acid and nicotinamide gave rise to a 2- to 3-fold elevation of plasma corticosterone in the intact rat. This effect was abolished by hypophysectomy. The plasma corticosterone response to nicotinamide injection was greatly delayed as compared with that of nicotinic acid, thus suggesting that the activity of nicotinamide is contingent upon prior conversion to nicotinic acid and possibly other active metabolites. 6-Amino-, 5-methyl-, and 5-fluoro-nicotinamide, nicotinylhydrazide, and isoniazid were also found to be potent stimulators of adrenocortical secretion. Our results indicate that these compounds exert their effect on adrenocortical secretion by a stimulatory effect on the pituitary output of ACTH.

A comparative survey of steroids and steroidogenic pathways throughout the vertebrates

Corticosteroid hormone biosynthesis has been demonstrated in most classes of vertebrates, both Agnatha and Gnathostomata. Though comparative steroid endocrinology is still a young discipline, it is possible to group, tentatively, the different classes of animals according to the chemical nature of the corticosteroid hormones elaborated. In many instances these results were obtained in vitro and only on a limited number of representatives of a class. Thus our classification is only preliminary. Group I. Animals that secrete both 17-hydroxylated (e.g., cortisol, cortisone, 11-deoxycortisol) and 17-deoxycorticosteroids (e.g., corticosterone, 11-deoxycorticosterone, 18-hydroxycorticosterone, aldosterone). Most mammals investigated belong to this group, including subeutherian and eutherian orders. Notable exceptions from this endocrine pattern are found in the order of Rodentia, and some amphibians, both urodeles ( Amphiuma) and anurans ( Bufo), can be included in this group. Group II. Animals that secrete only 17-deoxycorticosteroids. The group comprises Aves, Reptilia, amphibians (Ranidae), and the rat and mouse (Order Rodentia). Group III. Animals that secrete only 17α-hydroxycorticosteroids. The few orders of Osteichthyes investigated can be classified in this group, but with some reservations, as both corticosterone and aldosterone were reported in bony fishes. Group IV. This chemically heterogeneous group comprises mostly chondrichthians. In this class adrenocortical secretion seems to vary from order to order. Thus, in the genus Raja the main, and possibly only, secretory product is 1-α-hydroxycorticosterone; the elaboration of cortisol was reported in the ratfish ( Hydrolagus), and of corticosterone in dogfishes ( Squalus and Mustelus). This tentative classification demonstrates that for adrenocortical secretion the same chemical building-blocks are used throughout the vertebrates. No quantitative classification has been attempted. Studies on the biosynthesis of steroid hormones in mammalian adrenals are numerous, but few reports exist on biosynthetic routes operating in the adrenals of nonmammalian vertebrates. The pathway acetate-cholesterol corticosteroids was shown to exist in birds, and the route cholesterol-corticosteroids in one species of bony fish ( Anguilla). Pregnenolone and progesterone are precursors of both 17-hydroxy and 17-deoxycorticosteroids in all four groups. Aldosterone is biosynthesized from corticosterone in all aldosterone-producing species; it is accompanied in most instances by the production of 18-hydroxycorticosterone. On the intracellular level, adrenal mitochondria were shown to be the main source of steroid 18-oxygenating enzymes in Mammalia, Aves, and Amphibia. These synthetic routes are found in mammalian adrenals as well. Thus there seems to be a basic uniformity in steroid biochemistry in all hormone-producing adrenal cells. The adrenal itself shows progressive evolution from the scattered secretory cells in fishes to the encapsulated and zonated organ in mammals, but no evolutionary trend is yet apparent in the chemical nature of adrenocortical secretion. Nor can obvious connections be seen between the type of hormone synthesized and the habitat of the animal. The full potential of steroid hormone biosynthesis may have been acquired with the development of an inner supporting structure, and from this pool of possible reactions each class, order, or genus may have adopted biosynthetic routes to solve its adaptive and metabolic problems.

Experimental studies on the effect of low oxygen inhalation on adrenocortical secretion--by the retention cannula method for collecting lumbo-adrenal venous blood in the dog

本研究は犬副腎静脈カニューレ留置のもとで, 諸段階の低酸素家呼吸の副腎皮質ホルモン分泌に及ぼす影響を観察した.その結果10% O2, 7% O2と低酸素の強度に従って, 副腎皮質ホルモンの分泌増加を認めたが, 5% O2吸入では7% O2吸入時よりむしろ反応が弱かった.HypoxiaがStressとして間脳・下垂体を介してACTH分泌を促すものであり, 測腎皮質反応の低酸素呼吸におけるthreshold pointが7%と5% O2のあたりにあると考えられる.

Inhibition of the response to pituitary adrenocorticotrophic hormone in the hypophysectomized rat by circulatory corticosterone.

SUMMARY The adrenal response to adrenocorticotrophin (ACTH), as determined by the secretion of corticosterone into adrenal vein blood,was measured in hypophysectomized rats in the presence of low and high levels of corticosterone in the peripheral circulation. To ensure that the level of corticosterone was low in the peripheral blood, the animals were hypophysectomized 24 hr. before the experiment, and one adrenal was removed before the start of infusion of ACTH. After the onset of the infusion the effluent from the remaining gland was collected in a receptacle, thus preventing any corticosterone produced under the influence of ACTH from reaching the general circulation. To study the effect of a high level of circulating corticosterone on the adrenal response to ACTH, corticosterone was injected subcutaneously, in beeswax and arachis oil, before the start of infusion of ACTH. In these experiments, too, the steroid secreted under the influence of ACTH was prevented from entering the general circulation. The peripheral levels attained by the injection of corticosterone were within the range observed during surgical stress, i.e. about 40 μg./100 ml. blood. When the corticosterone levels were within this range the response to a continuous infusion of ACTH was reduced by approximately 22% when compared with animals which had received no corticosterone and whose peripheral corticosterone levels were hardly measurable. These results suggest that corticosterone is probably involved in a direct feedback mechanism of adrenocortical secretion in the rat as its inhibitory effect on the response to ACTH can be demonstrated at peripheral levels of corticosterone which are within the range found during surgical stress.

Circadian adrenal rhythm in diabetics.

The circadian rhythm of adrenocortical secretion in 18 diabetic subjects was normal as judged by serial plasma 11-OH-corticosteroid levels. Mild episodes of hypoglycaemia induced a rise in the plasma 11-OH-corticosteroid in 12 diabetic patients on insulin therapy.

Effect of Smoking and Nicotine on Adrenocortical Secretion

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.

Effect of smoking and nicotine on adrenocortical secretion

Effect of smoking and nicotine on adrenocortical secretion

The dynamics of adrenocortical secretion.

The dynamics of adrenocortical secretion.

EFFECT OF SMOKING AND NICOTINE ON ADRENOCORTICAL SECRETION

Journal Article EFFECT OF SMOKING AND NICOTINE ON ADRENOCORTICAL SECRETION Get access Alfred Kershbaum, Alfred Kershbaum Division of Cardiology, Philadelphia General Hospital, 34th St. & Curie Ave., Philadelphia, Pennsylvania 19104, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar Douglas J Pappajohn, Douglas J Pappajohn Division of Cardiology, Philadelphia General Hospital, 34th St. & Curie Ave., Philadelphia, Pennsylvania 19104, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar Samuel Bellet, Samuel Bellet Division of Cardiology, Philadelphia General Hospital, 34th St. & Curie Ave., Philadelphia, Pennsylvania 19104, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar Masami Hirabayashi, Masami Hirabayashi Division of Cardiology, Philadelphia General Hospital, 34th St. & Curie Ave., Philadelphia, Pennsylvania 19104, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar Hassan Shafiiha Hassan Shafiiha Division of Cardiology, Philadelphia General Hospital, 34th St. & Curie Ave., Philadelphia, Pennsylvania 19104, U.S.A. Search for other works by this author on: Oxford Academic Google Scholar Acta Endocrinologica (Norway), Volume 56, Issue 1_Supplement, Dec 1967, Page S41, https://doi.org/10.1530/acta.0.056S041 Published: 01 December 1967

CIRCADIAN STUDIES ON PLASMA CORTISOL IN SUBJECTS WITH PEPTIC ULCER

It has been suggested by Selye (1951) and Gray & Ramsey (1957) that the adrenal cortex and centres regulating its function may be involved not only in the physiological control of gastric secretion but also in the aetiology of peptic ulceration. This possibility became of great interest after the introduction of corticosteroids into clinical practice; long-term treatment has been reported to have, as a side-effect, a high incidence of peptic ulcers which are similar to spontaneous ones (Garb, Soule, Bartholomew & Cain, 1965). Determinations of plasma concentration and urinary excretion of corticosteroids in patients with peptic ulcer failed to detect differences from normal subjects. However, it is likely that the quantitative changes in cortical activity may be too subtle to be shown by this type of test: they may only be demonstrable by following the circadian fluctuations in adrenocortical secretion. The circadian changes in the plasma cortisol levels were therefore

Systems analysis in the study of homeostasis: with special reference to cortisol secretion

The systems analytic approach to complex problems by way of mathematical models and computer simulation is discussed. The relevance of this approach to the problem of homeostasis is considered. The partial success obtained to date through the application of the systems approach to a description of the control of adrenocortical secretion is described in some detail. This description attempts to indicate the successive and repeated interaction of the model and the experiment. In my opinion, such interaction is critical if the mathematical model is to be a useful and realistic description of the system, and if the experiments are to be designed in such a way that the results can generate useful information.

Effect of extracorporeal circulation and deep hypothermia on adrenocortical secretion.

Extracorporeal circulation and deep hypothermia (8–15 and 18–25 C, midesophageal temperature) induced in anesthetized dogs a marked decrease in adrenocortical secretions, as estimated by hydroxycorticosteroid (cortisol, corticosterone) and 17-ketosteroid levels in adrenal venous blood. After extracorporealextracorporeal rewarming, the blood levels of these compounds increased toward control values. The rate of return varied according to the thermal level and the type of steroid. The selective influence of cold on the enzyme systems involved in adrenocortical steroid biosynthesis is discussed. {Endocrinology 80: 1174,1967)

Influence of thymectomy on plasma corticosterone in the rat

The hypothesis that previously reported differences between thymectomized and sham thymectomized rats are related to an influence of thymectomy on adrenocortical secretion was examined. Plasma corticosterone was determined before surgery, 1, 7, 14, and 21 days after surgery, and again after 20 IU and 120 IU of ACTH, in thymectomized, sham thymectomized and unoperated control male rats. Corticosterone was elevated throughout the study in all operated animals. No differences between thymectomized and sham thymectomized rats were observed. ACTH reduced weights of accessory reproductive structures of thymectomized, sham thymectomized and unoperated rats.

Effect of a Low Sodium Diet on Aldosterone-Stimulating Activity Of Angiotensin II in Dogs

SummaryThe effect of various doses of angiotensin II on adrenocortical secretion of aldosterone and 17-hydroxycorticoids was determined in dogs fed a low sodium diet for 14 days and in control dogs. The increments in aldosterone secretion produced by angiotensin II in the animals fed the low sodium diet were greater than the corresponding increments in controls. No changes in the increments in 17-hydroxycorticoids or blood pressure were observed.Angiotensin II (1-L-asparaginyl-5-L-valyl angiotensin octapeptide) was provided by Ciba Pharmaceutical Co., Summit, N. J. ACTH was provided by Upjohn Co., and Lonalac for preparation of low sodium diets by Mead Johnson Co. We wish to thank Mr. Roy Shackelford and Miss Margaret Saari for technical assistance.

Effect of tranylcypromine on adrenocortical secretion in the dog.

Tranylcypromine in doses of 2 mg/kg or more inhibits the output of 17-hydroxycorticoids from the adrenal following administration of ACTH in the dog. This drug, which has been used clinically as an antidepressant, does not interfere with the Porter-Silber method. The increase in 17-hydroxycorticoid secretion produced by angiotensin II is also inhibited. ACTH secretion is not inhibited. The drug reduces the output of cortisol and 11-deoxycortisol while increasing that of corticosterone, 11-deoxycorticosterone and aldosterone. This suggests that it acts by inhibiting adrenocortical 17α-hydroxylase. (Endocrinology 80: 510, 1967)

The effect of 4,4'-methylenedianiline on adrenal corticosterone secretion in the rat.

The effect of 4, 4'-methylenedianiline on the adrenocortical secretion in the rat was investigated. Under sodium pentobarbital anesthesia, adrenal venous blood was collected through a polyethylene cannula inserted into the adrenal vein and analyzed for corticosterone. 4, 4'-Methylenedianiline dihydrochloride was administered intravenously in a dose of 100mg/kg. In non-hypophys-ectomized rats, the increased corticosterone secretion in response to surgical stress caused by the adrenal vein cannulation was markedly depressed following the injection of methylenedianiline. A low secretion rate of corticosterone persisted for 30 minutes thereafter. In hypophysectomized rats, the increased corticosterone secretion produced by intravenous infusion of ACTH was also markedly depressed by injection of methylenedianiline. It is thus concluded that in the rat the adrenal corticosterone secretion is depressed by 4, 4'-methylenedianiline and that this inhibitory effect on adrenal corticosterone secretion is due to a direct action of the drug on the adrenal cortex.

On the Mechanism of Stimulatory Action of Histamine upon the Adrenal 17-Hydroxycorticosteroid Secretion in the Dog

Under sodium pentobarbital anesthesia adrenal venous blood was collected from intact, bilaterally splanchnicotomized and hypophysectomized dogs and was analyzed for 17-hydroxycorticosteroids (17-OHCS). Adrenal 17-OHCS secre-tion in response to histamine in intact dogs anesthetized with pentobarbital was not different from that in conscious ones. Section of the splanchnic nerves did not alter the adrenocortical secretion response to histamine, whereas hypo-physectomy abolished or markedly depressed the 17-OHCS secretion response. These results suggest that the adrenal 17-OHCS secretion in response to histamine in the dog is mainly mediated through pituitary adrenocorticotrophin release and it is due neither to psychic excitement producible by histamine administration nor to adrenomedullary hormone release.

In vitro effect of adrenocorticotropin on corticoid secretion in the turtle, snake, and bullfrog

The regulation of corticosteroid secretion was investigated in vitro in two genera of turtle ( Pseudemys spp. and Emys orbicularis ), the snake ( Natrix natrix ), and the bullfrog ( Rana catesbeiana ). Pseudemys adrenal tissue produced aldosterone and corticosterone in addition to a quantitatively prominent unidentified α ketol- Δ 4 -3 ketosteroid and responded to Wilson ACTH by increasing adrenocortical secretion approximately 40%. Emys and Natrix adrenals converted progesterone-4-C 14 to aldosterone and corticosterone, and the snake also yielded three unidentified labeled α ketol- Δ 4 -3 ketosteroids. In both species, corticosterone was the major product of conversion and endogenous secretion. Wilson ACTH increased by 250% the conversion of labeled progesterone to aldosterone by Emys adrenals. However, this represented only a 20% total increase in the incorporation of C 14 into corticoids since labeling of corticosterone was unaffected. The effect of Wilson ACTH, Bell ACTH peptides, or snake anterior pituitary preparations on corticoid biosynthesis by Natrix adrenals in the presence of precursor progesterone, although equivocal, was not substantial at best. Mammalian ACTH increased adrenocortical secretion in Rana two to six-fold. The present findings suggest that the reptilian adrenal is fairly unresponsive to ACTH stimulation under the in vitro conditions employed.