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PubMed1956

The action of corticotropin (ACTH) on nucleic acids and subcellular elements of the adrenal cortex.

It was shown experimentally that ACTH causes an increase of cytoplasmic RNA and subcellular granules of the adrenal cortex shortly after administration. This effect was found to be concentrated primarily on the basophilic cytoplasmic granules and to be largely independent of cell division. The increase of nuclear RNA, DNA, and nuclear mass followed that of the cytoplasm. The observations indicate also that the mass increase of mitochondrial and chromidial systems is closely related to the increase in cytoplasmic, largely chromidial RNA.

Adrenal Cortex↗
PubMed1955

Effects of corticosterone, hydrocortisone, and corticotropin on production of antibodies in rabbits.

The effects of hydrocortisone, corticosterone, and pituitary adrenocorticotropin on antibody production were studied immunochemically in rabbits. Hydrocortisone in doses as low as 2.5 mg. per day (approximately 1.0 mg. per kg. per day) markedly depressed antibody production whereas corticosterone in doses four times as large exerted no significant effect. Corticotropin in doses of 15 units daily exerted an effect similar to that of corticosterone, but its effect was more like that of hydrocortisone when given in doses twice as great. This finding is in agreement with observations that the prolonged administration of corticotropin in sufficient dosage leads to increased output of hydrocortisone by the adrenal cortex of the rabbit. Corticosterone did not antagonize the effect of hydrocortisone on antibody production, but seemed to act additively with it. Although each of the hormones tested induced some adverse effect on nitrogen balance as measured by the weights of the animals, and hydrocortisone induced the more striking decreases in weight, there was no direct correlation between the effects of these hormones on antibody production and their effects on weight.

Adrenal Cortex↗
PubMed1957

The influence of adrenocorticotropic and growth hormones on antibody formation.

The influence of pituitary adrenocorticotropic hormone (ACTH) and growth hormone (somatotropin, STH), singly and in combination, has been studied in normal, young adult rats, with respect to antibody formation against Fraction IA of Pasteurella pestis. When ACTH was administered during the period of immunization, in a daily dose just sufficient to prevent body weight increase relative to the non-treated, immunized controls, serum antibody levels against the specific antigen employed were significantly depressed. The administration of STH alone resulted in a marked increase in body weight. The increase in antibody level was not significant at the 5 per cent level when compared with the control values. The same dosage of STH given simultaneously with ACTH maintained body weight at a level slightly above that of the controls, and resulted in an effective counteraction of the antibody depression produced by the latter hormone.

Adrenocorticotropic Hormone↗
PubMed1957

Corticotropins (ACTH). X. Biological investigations on alpha-corticotropin.

Purified alpha-corticotropin has been reported to exercise the following biological effects: (a) stimulation of the adrenal glands in normal and hypophysectomized rats, (b) production of blood eosinopenia in hypophysectomized rats, (c) maintenance of muscle glycogen in hypophysectomized rats, (d) inhibition of growth-promoting activity of somatotropin, (e) stimulation of melanocytes in the skin of frogs, (f) mobilization of fat into the liver of fasted mice, (g) stimulation of the accessory sex glands of castrated-hypophysectomized male rats, (h) induction of deciduoma formation in hypophysectomized-oophorectomized rats, and (i) elevation of the total red cell volume in hypophysectomized rats. alpha-Corticotropin has also been shown for the first time to act in synergism with lactogenic hormone as an essential galactopoietic hormone. The ability of alpha-corticotropin to elicit biological responses in the absence of the adrenal cortex is discussed.

Adrenocorticotropic Hormone↗
PubMed1957

Effect of pituitary adrenocorticotropic and growth hormones on the resistance of rats infected with Pasteurella pestis.

The influence of highly purified pituitary adrenocorticotropic (ACTH) and growth (somatotropic, STH) hormones on resistance of normal, young adult rats infected with Pasteurella pestis organisms (EV 76) has been studied. The daily dosage of ACTH was 0.1 mg. (25 I.U per mg.) and that of STH was 1.0 mg. When these hormones were administered for 3 days prior to infection (1 LD(50)) and for 4 days thereafter, ACTH treatment resulted in a significant depression of resistance (p = < 0.001). The simultaneous administration of STH not only resulted in a definite counteraction of the depression (p = < 0.001), but resistance was increased to a level significantly above that of the non-hormone treated controls (p = < 0.001). Treatment with STH alone also showed a significantly higher protection when compared to the same controls (p = < 0.05). The results of experiments in which the challenge dose was 1 LD(50) suggested that greater alterations in resistance, whether it be a depression or enhancement, could be obtained by continuing hormone treatment after challenge instead of discontinuing on the day prior to challenge. When animals were treated with a relatively high daily dose (1.0 mg.) of ACTH and challenged with only (1/4) of an LD(50) of organisms, the majority of animals died within 4 to 7 days, whereas either the ACTH treatment or the bacterial dose alone resulted in no deaths. If the hormones were administered for 2 weeks prior to challenge with a high, toxic dose of organisms (4 LD(50)), and discontinued thereafter, there were significant differences in mortality in the various groups during the first 24 hours post challenge. The ACTH treated group showed a marked drop in resistance (p = < 0.001). STH, when given alone, exercised a significant protection (p = < 0.02), and in combination with ACTH, effectively counteracted the depression of resistance to acute, toxic deaths induced by the latter hormone (p = < 0.001). In this particular experiment, practically all animals died within 4 to 5 days, owing to the high challenge dose; the few survivors were in the group that had been pretreated with growth hormone. The maximal loss in body weight following an LD(50) challenge dose occurred by the 3rd day post challenge in all groups except in the ACTH-treated animals. At this time the LD(50) control group had lost an average of 14 gm. per rat, the STH group only 3 gm. per rat, whereas the group receiving both hormones lost an average of 7.5 gm. per rat. The ACTH-treated animals showed the greatest weight loss on the 4th day. Thus, under the conditions of the experiment, the beneficial effect of STH on the maintenance of body weight was demonstrated during the period of acute infection. The peak incidence of death in controls or hormone-treated animals following infection with 1 LD(50) of living organisms occurred on the 4th to 5th day post challenge; the earliest deaths occurred on the 3rd day, while the latest occurred on the 7th day. The peak incidence of death after the 4 LD(50) challenge dose occurred earlier, falling on the 2nd to 3rd day. Death was always accompanied by the characteristic gross pathology which results from infection with Pasteurella pestis organisms, particularly in the animals which succumbed after the 3rd day. Bacterial cultures usually revealed the presence of numerous Pasteurella pestis organisms in the spleen and heart blood at the time of death.

Adrenocorticotropic Hormone↗
PubMed1951

The effect of adrenocorticotropic hormone on inflammation due to tuberculin hypersensitivity and turpentine and on circulating antibody levels.

The treatment with adrenocorticotropic hormone of guinea pigs sensitized with heat-killed tubercle bacilli caused suppression of their skin reactivity to tuberculin. Similar animals treated with saline did not show this change. Normal guinea pigs treated with adrenocorticotropic hormone showed suppression of inflammation, but not necrosis, produced by intracutaneous oil of turpentine. There was slight, but probably not significant, diminution of inflammation during saline administration. Tuberculin complement-fixing antibody titers were not altered by either adrenocorticotropic hormone or saline administration. Adrenocorticotropic hormone produced marked eosinopenia and lymphopenia in guinea pigs.

Adrenocorticotropic Hormone↗
PubMed1954

The effect of adrenal steroids, corticotropin, and growth hormone on resistance to experimental infections.

Cortisone acetate, hydrocortisone, and hydrocortisone acetate depress the resistance of mice to pneumococcal and influenza viral infections, although hydrocortisone acetate is somewhat less effective than the free alcohol, when given subcutaneously. Pituitary adrenocorticotropin, even in highly purified form and in oil and beeswax, does not significantly alter the resistance of mice to these experimental infections, even when given in doses which may cause profound eosinopenia, lymphopenia, and weight loss, and which are at the limit of tolerance of the animals. Corticosterone depresses resistance to pneumococcal infections significantly, but fails to alter resistance to influenza viral infections. The findings suggest that murine adrenals may produce one of the known adrenal steroids such as corticosterone along with another steroid, or may produce a steroid other than cortisone, hydrocortisone, or corticosterone. When resistance is decreased by adrenal steroids, survival time is invariably shortened, and the effect of the steroid hormones is frequently demonstrable within the 1st day after infection with pneumococci, making it unlikely that the depression of resistance that is seen is primarily due to depression of antibody formation. A single dose of 5 mg. of cortisone may cause depression of resistance and may decrease the survival time for 3 to 6 days afterward. Growth hormone (somatotropic hormone) in highly purified form, and in the doses used, did not overcome the weight loss induced by cortisone, but the animals treated with growth hormone and cortisone regained their lost weight more rapidly than those receiving cortisone alone. Growth hormone alone caused a slight increase in the rate of gain in weight over controls. Growth hormone alone did not increase resistance to infection, and did not increase the survival time, in mice infected with either pneumococci or influenza virus. Growth hormone in various dosages failed to overcome the effect of cortisone in depressing resistance to these infections. Cortisone, hydrocortisone, corticosterone, and corticotropin did not alter significantly the titers of influenza virus attained in the murine lungs during the first 2 days after infection, but cortisone and hydrocortisone markedly delayed the rate at which virus titers declined during the subsequent 6 days. Corticosterone and corticotropin delayed the rate at which the titers declined but slightly, and growth hormone had no apparent effect, as compared with controls. Growth hormone did not overcome the effect of cortisone and hydrocortisone on viral titers. No detectable antibody was found as late as 6 days after infection, in controls or in hormone-treated animals.

Adrenal Cortex↗
PubMed1954

The effect of ACTH and adrenal steroids on K transport in human erythrocytes.

The effect of ACTH and adrenal steroids on K transport in human erythrocytes has been studied. A new method of calculation has revealed that in normal human erythrocytes the K transport is not independent of external K concentration as had previously been thought. The equation describing the relationship is, K influx (m.eq./liter cells hour) = [K](pi)/(0.697 + 0.329 [K](pi)) in which [K](pi) refers to the plasma K concentration at the beginning of the experiment. At the physiological plasma K concentration of 4.65 m.eq./liter, K influx is 2.09 m.eq./liter cells hour; K efflux is 1.95 m.eq./liter cells hour and is independent of plasma K concentration. The effect of the infusion of ACTH and adrenal steroids on the K content of the erythrocytes was also studied. Infusions of ACTH or cortisone do not cause the expected loss in erythrocyte K content and may well cause a gain. Infusions of ACTH and cortisone decrease the rate of K influx and efflux slightly at all stages of the infusion, as measured in vitro in blood samples drawn at various times during and following the infusion. However, the erythrocytes incubated in vitro do not exhibit the same changes in K content as are found in vivo. Hydrocortisone added to normal cells in vitro also decreases both influx and efflux of K, without affecting the K content of the cells.

Adrenal Cortex↗