Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Isolated adrenal cells of rabbits aged from 0 h to day 40 after birth were incubated for 2 h in the presence of ACTH. Thin-layer chromatography and the fluorimetric method were used to evaluate the products of these adrenal cells separately for cortisol and corticosterone. Cortisol production by adrenal cells in response to ACTH (0.1 mU) was found to be highest between 0 and 8 h after birth (0.522 +/- 0.049 mug/105 cells; mean +/- SEM). A decrease was observed at 9-20 h and this was further followed by a steady decrease up to day 35-40. Corticosterone production was 0.206 +/- 0.042 mug/105 cells between 0 and 8 h after birth. Subsequently, this level was evenly maintained up to 12-14, but it tended to increase on day 35-40. The level of cortisol production was significantly higher than that of corticosterone production at 0-20 h after birth, while the former was significantly lower than the latter from day 12-14 onwards. The ratio of corticosterone to total corticosteroids (cortisol + corticosterone) was very low (0.28 +/- 0.04) at 0-8 h after birth, but showed a progressive rise up to day 35-40, when it was 0.95 +/- 0.01. The results of the present study show that cortisol is the pre-dominant product of the adrenal cells in rabbits during early post-natal life.
 ...
PMID:Cortisol and corticosterone productions of isolated adrenal cells in neonatal rabbits. 18 50

Plasma ACTH and corticosteroid concentrations were measured by radioimmunoassay in chronically catheterized fetuses of 32 pregnant sheep. Fetal plasma ACTH levels 38+/-5 pg/ml (means+/-SEM) were slightly (P < 0.05) lower than maternal 54+/-4 pg/ml levels. No general rise in fetal plasma ACTH concentration was noted before 140 days gestation; however, fetal plasma corticoid levels began to increase after about 125 days. This suggested that an increase in fetal adrenal responsiveness to endogenous ACTH occurred during gestation. Hemorrhage of 15% of estimated blood volume decreased mean arterial pressure from 54+/-3 to 36+/-3 torr and increased plasma ACTH from 30+/-5 to 130+/-30 pg/ml in fetuses older than 0.80 gestation. In fetuses younger than 0.67 gestation, 15% hemorrhage caused no change in plasma ACTH levels despite a significant fall in mean arterial pressure. This suggests that system(s) subserving the ACTH response to mild hemorrhage are either absent or nonfunctional in the younger fetuses. The hemorrhage-induced increase in plasma ACTH levels was associated with a small rise in plasma corticoids in fetuses younger than 0.94 gestation. In older fetuses, a similar increase in plasma ACTH was associated with a pronounced increase in plasma corticoid levels. This also suggests that an increase in adrenal responsiveness to endogenous ACTH occurs during gestation. No detectable changes in maternal plasma ACTH or corticoids were found in response to fetal hemorrhage, thus the fetal pituitary-adrenal axis can autonomously respond to stress.
 ...
PMID:Developmental aspects of the pituitary-adrenal axis response to hemorrhagic stress in lamb fetuses in utero. 20 13

Ten male mongrel dogs of 8.3-14.3 kg were bilaterally adrenalectomized and maintained on replacement steroids for 1 week. No exogenous steroids were detectable at the time of the experiment. Each dog, under light Nembutal anesthesia, received two stepwise primed constant infusions of cortisol (iv), each lasting 90 min (except in one dog with three infusions of 60 min). A recovery period of 80 min without cortisol infusion followed. Twenty-three venous blood samples were withdrawn for determination of plasma ACTH by adrenal cell suspension bioassay and 25 were withdrawn for plasma cortisol by fluorimetry at various times before, during, and after the cortisol infusions. ACTH secretion rates were calculated continuously from functions fitted to ACTH concentration and time data, using a validated single compartment approach with previously determined clearances and volumes. Initial high ACTH secretion rates of 1.0 +/- 0.2 mU/kg . min (range, 0.3-2.4) were reduced by 67.4 +/- 4.6% and 94.6 +/- 2.1% by the two cortisol infusions, which yielded cortisol plateau concentrations in plasma of 4.24 +/- 0.41 and 6.09 +/- 0.68 microgram/100 ml, respectively. This sensitive feedback response to low cortisol concentrations was delayed, with no effect for about 20 min and maximal effect reached within 1 h. There was no evidence of a fast rate-sensitive feedback. Some increases in ACTH secretion were seen during the recovery period (errors are +/- SEM).
 ...
PMID:Progressive suppression of adrenocorticotropin secretion in resting adrenalectomized dogs by low stepwise infusions of cortisol. 21 69

To define the nature of the disturbance of the corticosteroid feedback mechanism in Cushing's disease, the dynamic aspects of the ACTH response to corticosteroid administration have been studied in patients with Cushing's disease after total adrenalectomy (C.d. post adx.). The results were compared with those obtained in patients with Addison's disease (control group). Different experimental designs for administration of cortisol were chosen to provide extreme variations in the input signal. The response of the system was evaluated by measuring plasma ACTH concentrations (radioimmunoassay) at short time intervals. Infusion of cortisol at constant rate (50 mg/h for 2 h) resulted in a transient, paradoxical rise in ACTH levels with a maximum at 15 min. (315+/-65%, mean+/-SEM). In contrast, in the control group there was an immediate and rapid decrease in ACTH levels with a significant inhibition after 15 min (80+/-6%, mean+/-SEM). Infusion of 50 mg cortisol for 5 and 15 min, respectively, produced an increase in ACTH levels, which was confined to the time when cortisol levels were rising (maximum: 137+/-30% and 139+/-10% at 5 and 15 min, respectively, mean+/-SEM). This increase corresponded in time to the first decrease in ACTH levels in the Addisonian patients. With bolus injections of 25 mg cortisol, ACTH levels remained unchanged during the first 15 min. The time-course in the patients with C.d. post adx. was essentially the same as in the Addisonian patients. From these results it is concluded that in the patients with C.d. post adx. the rapid, rate-sensitive feedback mechanism was converted into a positive one, whereas the delayed, dose-sensitive mechanism was completely undisturbed. The capacity of dexamethasone to activate rate-sensitive feedback elements was markedly diminished. Accordingly, there were only minor positive feedback effects upon ACTH secretion in the patients with C.d. post adx.
 ...
PMID:Positive rate-sensitive corticosteroid feedback mechanism of ACTH secretion in Cushing's disease. 22 40

To provide clinical guidelines for the use of high-dose short-term glucocorticoid therapy, we studied recovery of the hypothalamic-pituitary-adrenal axis in 10 normal men following the administration of suppressive doses of prednisone (25 mg twice daily for five days). Cortisol responses to insulin-induced hypoglycemia and synthetic ACTH before treatment were compared with responses two and five days after concluding the prednisone course when adrenal function was not influenced by the presence of exogenous steroid. Two days after prednisone therapy, peak cortisol responses to both hypoglycemia (11.0 +/- 0.9 microgram/dl mean +/- SEM) and synthetic ACTH (13.3 +/- 1.4 microgram/dl) were significantly reduced compared to pretreatment (20.6 +/- 1.6 and 27.3 +/- 2.5 microgram/dl, respectively, p less than 0.001). Five days after concluding the prednisone therapy, peak cortisol response to hypoglycemia had returned to near pretreatment levels although peak cortisol response in the adrenal gland to synthetic ACTH (22.3 +/- 1.1 microgram/dl) remained reduced (p less than 0.05). These data suggest that brief courses of high-dose prednisone therapy may limit the adrenal component of the hypothalamic-pituitary-adrenal response to stress for up to five days.
 ...
PMID:Pituitary adrenal recovery following short-term suppression with corticosteroids. 22 43

Plasma ACTH levels in response to metyrapone and insulin hypoglycaemia were compared in subjects with normal pituitary-adrenal function. After a single dose of 2 g of metyrapone given with a snack at midnight, the ACTH level was 468 ng/l +/- 66 )SEM) at 07.30 h the next morning (mean increment approximately nine fold over normal morning values). After insulin-hypoglycaemia the peak ACTH level was 369 ng/l +/- 31 (SEM). Peak ACTH levels greater than 200 ng/l were achieved in twenty of twenty-one (95%) subjects after metyrapone and twenty of twenty-four (83%) after insulin. No major side effects were noted after metyrapone. It is concluded that the short single-dose metyrapone test produces at least as strong and consistent a stimulus to ACTH release as the standard insulin-hypoglycaemia test in normal subjects. A direct assay of ACTH avoids misinterpretations which are inherent in a judgement based on compound S increase only. The short test has significant practical advantages over the classical metyrapone test, and provides a convenient and sensitive method of assessing the negative feedback ACTH control mechanism. It may be particularly useful in detecting minor degrees of pituitary suppression. The value of this test in clinical practice for the investigation of patients with hypothalamic-pituitary diseases in comparison to the classical tests of ACTH stimulation has yet to be demonstrated.
 ...
PMID:The short metyrapone test: comparison of the plasma ACTH response to metyrapone and insulin-induced hypoglycaemia. 22 68

The effect of prostaglandin synthesis inhibition on basal and ACTH-stimulated adrenal and renal function was investigated in normal volunteers. Data were collected during control and experimental study periods (13 days each). Adrenocorticotrophic hormone (Cosyntropin, 80 U/day) was administered i.v. on days 8 and 9 of each period. Indomethacin (150 mg/day) was given on days 5 through 13 of the experimental period. The subjects ate a constant diet containing 9 mEq of sodium, 100 mEq of potassium, and 2,500 ml of fluid daily. Indomethacin markedly inhibited urinary PGE excretion and plasma PGE concentration. The effect of ACTH alone as compared to the effect of ACTH and indomethacin showed: plasma sodium concentration, 139 +/- 1 vs. 131 +/ 3 mEg/liter (P less than 0.01, mean +/- SEM); plasma osmolality, 287 +/- 3 vs. 270 +/- 3 mOsm/liter (P less than 0.01); free water clearance, 97 +/- 66 vs. -1100 +/- 380 ml/24hr (P less than 0.01); urine volume, 2,000 +/- 60 vs. 950 +/- 200 ml/day (P less than 0.01); and urine osmolality 282 +/- 12 vs. 720 +/- 144 mOsm/liter (P less than 0.01). We conclude that the effects of ACTH and prostaglandin synthesis inhibition interact to result in inappropriate antidiuresis.
 ...
PMID:Effect of indomethacin and adrenocorticotrophic hormone on renal function in man: an experimental model of inappropriate antidiuresis. 22 68

1. The effects of short-term (S.T., 30 min) and long-term (L.T., 4 days) administration of ACTH on peripheral blood corticosteroid levels and on in vitro steroidogenesis were investigated. 2. Control levels of cortisol, corticosterone and aldosterone were 58 +/- 12, 130 +/- 26 and 10 +/- 6 (SEM) ng/100 ml respectively. 3. Corticosterone was 70% higher after S.T. and 150% higher after L.T., when cortisol was 800% higher. 4. Adrenal homogenates from control echidnas converted [14C]progesterone predominantly to 11-deoxycorticosterone (45%) and 11-deoxycortisol (12%). 5. After L.T. the principal product was corticosterone (25%), but S.T. had no effect. 6. In control echidnas the Km and V for 11 beta-hydroxylation of 11-deoxycorticosterone were 20 microM and 2.8 rho mol/min/mg respectively. After L.T. V increased to 10 rho mol/min/mg.
 ...
PMID:The effects of ACTH on adrenal steroidogenesis and blood corticosteroid levels in the echidna (Tachyglossus aculeatus). 23 89

21-Hydroxylase congenital adrenal hyperplasia (21-OHCAH) involves a primary defect of the adrenal gland and a secondary involvement of ACTH secretion. The responses of the pituitary-adrenal axis to ovine CRH (oCRH, 1 micrograms/kg) were examined in subjects with different degrees of 21-OH deficiency. We studied 43 subjects: 7 classical and 6 nonclassical (NC) 21-OHCAH patients, 15 heterozygotes (HT) and 15 control subjects. Baseline plasma ACTH levels were higher in classical CAH than in NC-CAH, HT, and control subjects (mean +/- SEM, 66 +/- 14, 6 +/- 1.6, 4 +/- 0.5, and 5 +/- 0.5 pmol/L, respectively). The mean plasma ACTH response to oCRH in NC-CAH (17 +/- 3 pmol/L) was higher than in controls and HT (9 +/- 0.8 and 11 +/- 1.5 pmol/L). The highest ACTH responses to oCRH were obtained for classical CAH patients (126 +/- 29 pmol/L). Plasma cortisol rose after oCRH in control, HT, and NC-CAH patients but did not change in classical CAH. After oCRH, plasma 17-hydroxyprogesterone (17-OHP) were 4 +/- 0.5, 8 +/- 1.6, 93 +/- 28, and 359 +/- 110 nmol/L for controls, HT, NC-CAH, and classical patients, respectively. There was a significant correlation (r = 0.70) between 17-OHP and the ACTH responses to oCRH. The 17-OHP responses to oCRH were also correlated (r = 0.94) with the 17-OHP responses to the synthetic ACTH test. We conclude that the release of endogenous ACTH by oCRH result in graded 17-OHP responses on 21-OH deficiency. The present study also suggests that different degrees of adrenal biosynthetic defect may result in graded ACTH responses to oCRH.
 ...
PMID:Pituitary-adrenal responses to corticotropin-releasing hormone in different degrees of adrenal 21-hydroxylase deficiency. 130 66

Our previous observations have shown that calcitonin (CT) stimulates beta-endorphin, ACTH, and cortisol secretion. In order to give further information on the supposed hypothalamic pituitary involvement in this effect, we studied the influence of dexamethasone on this stimulative influence of CT. Six healthy women aged 50-65 years were investigated. All the subjects received 100 U CT salmon (Sandoz) i.v. at 0800 (0 time). Plasma beta-endorphin, ACTH, and cortisol were estimated every 30 min from -30 to 120 min by specific radioimmunoassays. The same subjects were evaluated a second time, at the same intervals, when 1 mg dexamethasone was administered per os at 11 PM the previous night and CT i.v. at 0800 the next morning. Beta-endorphin, ACTH, and cortisol levels (mean +/- SEM) rose significantly after 100 U CT from 5.6 +/- 0.17 to 16.75 +/- 1.8 pmol/L (p less than 0.001); from 39.6 +/- 6 to 88.0 +/- 3.1 pg/ml (p less than 0.0001) (from 8.7 +/- 1.3 to 19.4 +/- 0.7 pmol/L); and from 13.1 +/- 1.6 to 23.8 +/- 3.0 micrograms/dl (p less than 0.0001) [374 +/- 45 to 680 +/- 85 nmol/L], respectively. Dexamethasone suppressed almost completely the stimulatory effect of CT beta-endorphin rose from 4.9 +/- 0.12 to 6.3 +/- 1.3 pmol/L (n.s.), ACTH from 38.6 +/- 5.1 to 42.6 +/- 6.2 pg/ml (n.s.) (from 8.5 +/- 1.1 to 9.4 +/- 0.9 pmol/L) and cortisol from 0.88 +/- 0.23 to 0.88 +/- 0.18 microgram/dl (n.s.) (from 25.1 +/- 6.5 to 25.0 +/- 5.1 nmol/L).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Dexamethasone suppression of the calcitonin induced beta-endorphin, ACTH and cortisol secretion. 131 84


1 2 3 4 5 6 7 8 9 10 Next >>