Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ontogenetic renal responsiveness to exogenous cortisol was examined in the chronically cannulated ovine fetus. The contribution of effects at proximal and distal tubule of the kidney were studied also. Cortisol (81.5 micrograms/h) was infused into immature ovine fetuses (mean gestational age -113.9 days) on five occasions and increased blood cortisol from 0.8 +/- 0.5 to 21.3 +/- 6.2 nmol/liter. This dose of cortisol produced a highly significant diuresis and natriuresis, in part due to an increase in GFR and in part due to a significant decrease in proximal tubular reabsorption of sodium. Cortisol (107.2 +/- 4.7 micrograms/h) was infused into mature fetuses (mean gestational age 133.4 days) and produced an increase in blood cortisol concentration from 11.4 +/- 5.6 to 33.7 +/- 6.8 nmol/liter. No natriuresis or diuresis was seen in the mature fetuses. Cortisol caused a significant depression of proximal tubular sodium reabsorption in mature fetuses, but this extra load was reabsorbed in the distal tubule in these fetuses. The inability of the premature or very low birth wt baby to maintain normal sodium balance on a standard salt intake may be due, at least in part, to a "fetal" renal response to the high plasma cortisol concentrations found in such babies. As the kidney matures it becomes capable of increasing distal tubular sodium reabsorption to compensate for any increased distal tubular fluid delivery.
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PMID:Gestational changes in renal responsiveness to cortisol in the ovine fetus. 277 10

Cortisol had a biphasic action on GABAA-receptor-mediated contractile responses, enhancing at picomolar concentrations (1-10 pM) and inhibiting at higher concentrations (10-1000 nM). There was a sinistral shift of the GABA dose-response curve in the presence of 10 pM cortisol, with a significant potentiation of the GABA-induced contractions over the lower dose range of GABA (3-30 microM), whereas 100 nM cortisol caused a non-parallel dextral shift of the GABA dose-response curve, with a depression of the maximum GABA response indicative of non-competitive antagonism. Cortisol at various concentrations did not affect GABAB-receptor-mediated ileal relaxations, or the baclofen-induced depression of twitch contractions to transmural stimulation. Such concentrations of cortisol also did not affect ileal responses to exogenously applied acetylcholine or cholinergic twitch contractions themselves. These results suggest that cortisol is a specific, and very potent modulator at GABAA-receptor complexes in the guinea pig ileum.
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PMID:Cortisol: a potent biphasic modulator at GABAA-receptor complexes in the guinea pig isolated ileum. 282 68

The Hamilton Depression Rating Scale (HDRS) score and plasma cortisol values were measured in 100 depressed patients at 8 a.m., 4 p.m. and 11 p.m. after oral administration of 1 mg dexamethasone the previous night. The patients were categorized according to DSM-III as suffering from either minor depression (including dysthymic disorder, 300.40; adjustment disorder with depressed mood, 309.00; atypical depression, 296.82) or major depression (without melancholia, 296.X2; with melancholia, 296.X3; with psychotic features, 296.X4). Plasma cortisol levels of greater than or equal to 3.5 micrograms/dl at 8 a.m. were found to be the most sensitive (56.9%) and specific (94.3%) discriminator between minor and major depression. Plasma cortisol levels at 4 p.m. and 11 p.m. or the combination of several cortisol values also differentiated between minor and major depression; however, the results were not so conclusive. According to the ratings on the Hamilton Depression Scale the patients with major depression were more severely depressed (P less than 0.001) than patients suffering from minor depression. Cortisol values at 8 a.m., 4 p.m., 11 p.m. and the highest levels were significantly (P less than 0.001) correlated with the HDRS score. A maximum of 20.2% of the score variance could be explained by the correlation with the highest cortisol value observed. Severity of illness does not exclusively account for the biological differences between minor and major depression.
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PMID:The dexamethasone suppression test, the Hamilton Depression Rating Scale and the DSM-III depression categories. 294 74

Forty outpatients with major depressive disorder were studied with the 1 mg DST and the Afternoon Cortisol Test. No relationship was found between hypothalamic-pituitary-adrenal (HPA) axis function and Research Diagnostic Criteria subtypes of depression, with the exception of higher log post-dexamethasone cortisol levels in endogenous depressives. Patients with mood reactivity had lower cortisol values on all assessments. The data suggest that the presence of mood reactivity may be useful as a predictor of normal HPA function in depression.
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PMID:Clinical variables and hypothalamic-pituitary-adrenal function in depression. The importance of mood reactivity. 295 6

The dexamethasone suppression test was performed in 63 depressed patients and 43 normal controls. Cortisol nonsuppression was found in 47.6% of the depressed patients and 4.6% of the controls. Among depressed patients both age and reported weight loss, but not severity of depression, were significantly related to postdexamethasone plasma cortisol levels. Patients who were cortisol suppressors had experienced significantly more life events before the onset of depression and had significantly higher hostility scores on a personality questionnaire than cortisol nonsuppressors.
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PMID:Cortisol nonsuppression in depression: relationship to clinical variables. 296 88

Synthetic ovine corticotropin releasing factor (o-CRF) was administered as an intravenous bolus (100 micrograms) to eight patients suffering from a major depressive disorder, endogenous subtype. All patients showed inadequately suppressed cortisol levels after 1 mg dexamethasone. After clinical remission and normalized dexamethasone responses, these patients were reinvestigated with o-CRF stimulation. The mean adrenocorticotropic hormone (ACTH) release from the pituitary corticotroph cells was indiscriminate at both test sessions. Cortisol and corticosterone output after o-CRF tended to be higher during depression than after recovery. The o-CRF-induced increments observed with corticosterone were more marked in comparison with cortisol. Within the limitations of the current protocol, our preliminary data lend support to the view that an increased pituitary ACTH reserve or adrenocortical steroid reserve is not likely to be responsible for the defective pituitary-adrenal regulation in some dexamethasone-resistant depressives.
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PMID:ACTH, cortisol, and corticosterone output after ovine corticotropin-releasing factor challenge during depression and after recovery. 298 88

The current study was designed to investigate whether glucocorticoid output after syn-ACTH stimulation is different in depression associated with dexamethasone suppression test (DST) nonsuppression from the euthymic state and DST suppression. We gave 28 depressives a DST and an adrenocortical challenge with synthetic ACTH. Fourteen patients were nonsuppressors on the DST. After successful drug treatment, the subjects were reinvestigated by both tests; all DSTs revealed plasma cortisol concentrations below the criterion value of 50 ng/ml. Cortisol and corticosterone responses after syn-ACTH tended to be higher during depression. After clinical remission, higher cortisol and corticosterone responses occurred in those patients who were DST nonsuppressors during depression. This finding suggests that patients who suffer from a depression which is linked to an abnormal pituitary--adrenocortical regulation develop an enhanced sensitivity of the adrenal cortex to ACTH.
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PMID:Cortisol and corticosterone response after syn-corticotropin in relationship to dexamethasone suppressibility of cortisol. 301 21

Concentrations of hydrocortisone as low as 0.08 microgram/ml significantly reduced the yields of gamma-interferon (IFN-gamma) when phytohemagglutinin (PHA) or concanavalin A (ConA) were used as inducers; however, when staphylococcal enterotoxin A was utilized, higher concentrations (5.0 micrograms/ml) were required to achieve the same effect. Yields of interleukin-2 (IL-2) and lymphotoxin were also found to be sensitive to the effects of the steroids, but expressions of TAC antigen was not generally affected by these agents. In contrast to the effects of steroids on cell proliferation, lymphokine production remained suppressed after steroid withdrawal. Hydrocortisone appeared to influence the concentrations of cyclic nucleotides following lectin stimulation, but attempts to correct these alterations or to add exogenous IL-2 failed to restore lymphokine production to normal levels. Addition of the calcium ionophore A23187 partially restored IFN-gamma production. We conclude that the effects of corticosteroids on the yields of lymphokines, including IFN-gamma, are profound. The depression of lymphokine production appears to be associated with a number of alterations in the cell, including depression of protein synthesis, alterations in cyclic nucleotides, and diminution of the production of cofactors necessary for IFN-gamma production. Enhancement of the flux of calcium into the cell may restore some of the ability to produce IFN-gamma.
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PMID:The effect of hydrocortisone on the production of gamma-interferon and other lymphokines by human peripheral blood mononuclear cells. 302 73

The effects of cortisol on noradrenaline (NA)-induced responses of neurons in the parvocellular division of the paraventricular nucleus (PVN) were investigated in hypothalamic slices of rats. Cortisol (10(-5) M)-induced excitation in 7 out of 11 PVN neurons tested and inhibited 3 out of 8 PVN neurons which were not affected by NA. Cortisol alone did not affect the basal firing rate of the PVN neurons. We conclude that cortisol may have an inhibitory effect on neurons in the parvocellular division of the PVN through depression of the noradrenergic system.
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PMID:Cortisol suppresses noradrenaline-induced excitatory responses of neurons in the paraventricular nucleus; an in vitro study. 317 87

Although eating disorders of the bulimic type have been known for a long time, "bulimia nervosa" as a special and specific type of eating disorder was described only during the last decade. Clinical evidence has shown an increase in bulimic disturbances during the last few years. About 30% of the bulimic disturbances begin between the 14th and 18th year of age. About 50% of patients with bulimia nervosa have been anorexic before. A group of 30 patients with anorexia nervosa and a group of 11 patients with bulimia nervosa were compared by means of the dexamethasone suppression test and two depression scales at the beginning of inpatient treatment, after 8-12 weeks of inpatient treatment and at discharge. Patients with anorexia nervosa revealed significantly higher cortisol levels at the beginning of inpatient treatment as compared with the bulimic group. Cortisol levels were normalized with weight gain. Therapeutic measures in bulimia nervosa comprise medical and psychotherapeutic methods.
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PMID:[Bulimia nervosa in adolescence]. 322 86


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