Inhibition of Cyclic-AMP Phosphodiesterase in Human Lymphocytes by Physiological Concentrations of Hydrocortisone

Lavin, Norman; Rachelefsky, G.; Kaplan, Stanley A.

doi:10.1055/s-0028-1093750

Cited by 14 publications

(3 citation statements)

References 6 publications

(7 reference statements)

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“…It is also of interest that in the present study, the steroid anti-inflammatory agents caused a small inhibition of histamine release induced by compound 48/80 and immunological challenge, as was found for antigenevoked histamine release from human skin (Greaves & Plummer, 1974), since it has been suggested, from studies on human lymphocytes, that such compounds can likewise increase cyclic AMP levels by phosphodiesterase inhibition (Lavin, Rachelefsky & Kaplan, 1975). However, the aspirin-like drugs were very potent inhibitors of histamine release induced by the ionophore A23187, suggesting that other mechanisms may also operate; an increase in cyclic AMP levels, either by phosphodiesterase inhibitors or dibutyryl analogue of cyclic AMP, is not thought to prevent ionophore-induced histamine release (Garland & Mongar, 1976).…”

Section: Discussionmentioning

confidence: 93%

The Inhibition of Histamine Release From Rat Peritoneal Mast Cells by Non‐steroid Anti‐inflammatory Drugs and Its Reversal by Calcium

Lewis

Whittle

1977

British J Pharmacology

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1The non-steroid anti-inflammatory drugs, indomethacin, flufenamate and meclofenamate, inhibited the release of histamine from rat peritoneal mast cells induced by pharmacological or immunological challenge in vitro. 2 Anti-inflammatory steroids had little effect on histamine release from the mast cells. 3 Th inhibition of histamine release by the aspirin-like drugs was not prevented by incubation with glucose, unlike the inhibition of 2,4,dinitrophenol or antimycin-A. This suggests that the non-steroid anti-inflammatory compounds do not act by preventing the energy production from oxidative metabolism, required for histamine release. 4 The inhibition of the calcium ionophore A23187-induced histamine release by the aspirin-like drugs was reversed by an increase in the calcium concentration of the incubation medium. 5 The results suggest that the non-steroid anti-inflammatory compounds inhibit histamine release by actions on calcium influx into the mast cell, or on calcium mobilization or utilization within the mast cell.

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Section: Discussionmentioning

confidence: 93%

The Inhibition of Histamine Release From Rat Peritoneal Mast Cells by Non‐steroid Anti‐inflammatory Drugs and Its Reversal by Calcium

Lewis

Whittle

1977

British J Pharmacology

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“…The enhanced ability of the glucocorticoid-exposed cells to increase their cAMP level in response to acute hormonal stimulation apparently may result from various mechanisms. Thus, the glucocorticoid treatment has been found to cause both an elevated P-adrenoceptor number (Mano et al 1979;Fraser & Venter 1980;Hadcock & Malbon 1988), an increased abundance of the stimulatory guanine nucleotide binding protein, Gs (Rodan & Rodan 1986;Chang & Bourne 1987), an increased adenylate cyclase activity (Johnson & Jaworski 1983;Rodan et al 1984) and a lowered phosphodiesterase activity (Manganiello & Vaughan 1972;Lavin et al 1975;Redshaw 1980;Elks et al 1983;Christoffersen et al 1984). In most cases studied, these gluco-corticoid-induced modulations of cAMP metabolism develop slowly, but acute effects have also been reported (Mendelsohn et al 1973;Durant et a].…”

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confidence: 99%

Studies of Glucocorticoid Enhancement of the Capacity of Hepatocytes to Accumulate Cyclic AMP

et al. 1989

Pharmacology & Toxicology

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Pretreatment of cultured rat hepatocytes with dexamethasone markedly enhanced the acute cAMP response to glucagon, isoproterenol or forskolin. The effect of dexamethasone was apparent within 3-6 hr and was maximal after 20-30 hr. The amplification of the cAMP response to glucagon could also be produced by other glucocorticoids, with relative potency dexamethasone much greater than methylprednisolone greater than hydrocortisone. The increased cAMP response was associated with a reduced cAMP phosphodiesterase activity in cell lysates and a reduced effect of the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine in intact cells, indicating that the glucocorticoid pretreatment reduced cAMP degradation. However, the increase in response to glucagon in glucocorticoid-treated cells was relatively larger than the increase in forskolin response and also larger than the decrease in phosphodiesterase activity, suggesting that other factors in addition to down-regulation of phosphodiesterases was responsible for the effect. Cycloheximide abolished the difference in phosphodiesterase activity and cAMP response between dexamethasone-treated and control cells. The results suggest that the glucocorticoids increase the ability of hepatocytes to accumulate cAMP due to protein synthesis-dependent processes which at least in part involve reduced degradation of cAMP.

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“…Both thyroid and glucocorticoid hormones, accelerators of lung maturation, have been shown to increase cyclic AMP (CAMP) levels, albeit through different mechanisms. Glucocorticoids have been shown to elevate cAMP levels by inhibiting cAMP phosphodiesterase (23, 220,320,371), and thyroid hormones by stimulation of adenylate cyclase (224). This ability of glucocorticoids to increase cAMP levels has been verified in the fetal rabbit lung (21, 22, 23).…”

Section: Interactions Of Thyroid Hormones and Glucocorticoidsmentioning

confidence: 99%

Lung development and the pulmonary surfactant system: Hormonal influences

Hitchcock

1980

Anat. Rec.

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The effect of hormones on developmental events is not a new area of scientific investigation. However, in the last decade, the developing lung has been the focus of an increasing amount of basic and applied research. Inadequate development of the newborn's respiratory system precludes extra-uterine existence; indeed, such respiratory inadequacy has been a leading cause of death in premature infants. Tremendous strides have been made in understanding the basic cell biology of the developing lung. Much has been learned about the source, composition, and function of pulmonary surfactant, a surface-active material produced by the lung and essential to alveolar stability. Deficient stores of this material is a major etiologic factor in the respiratory distress syndrome of the newborn (RDS). This fact, coupled with observations that certain hormones can accelerate lung development and the consequent availability of adequate stores of pulmonary surfactant, has led to a large body of literaturae dealing with the effects of hormones (and other agents) on lung development. It is the purpose of this literature review (1) to discuss the various kinds of investigations which have linked surfactant synthesis to the type II pulmonary epithelial cell; and (2) to review the current status of research dealing with the effects of glucocorticoids and thyroid hormones on lung maturation.

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Inhibition of Cyclic-AMP Phosphodiesterase in Human Lymphocytes by Physiological Concentrations of Hydrocortisone

Cited by 14 publications

References 6 publications

The Inhibition of Histamine Release From Rat Peritoneal Mast Cells by Non‐steroid Anti‐inflammatory Drugs and Its Reversal by Calcium

The Inhibition of Histamine Release From Rat Peritoneal Mast Cells by Non‐steroid Anti‐inflammatory Drugs and Its Reversal by Calcium

Studies of Glucocorticoid Enhancement of the Capacity of Hepatocytes to Accumulate Cyclic AMP

Lung development and the pulmonary surfactant system: Hormonal influences

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