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At least 19 recordsLinked to original sources
PubMed1975

Quantitative ultrastructural study of the adrenal cortex: effects of a mammotropic pituitary tumor producing growth hormone and prolactin (MtT-W10), and of injected growth hormone in the rat.

The ultrastructure of the adrenal cortex has been examined in animals bearing a growth hormone and prolactin secreting mammotropic tumor (MtT-W 10). The large quantities of hormone secreted by the tumor caused a stimulation of zona fasciculata cells. The adrenal weight increased approximately 2-fold in tumor bearing animals. There were increases in the cellular volume of zona fasciculata cells and in the volume of mithchondria and smooth endoplasmic reticulum per cell as determined by quantitative morphometric techniques. The surface area of smooth endoplasmic reticulum and total mitochondrial membranes showed a significant increase in zona fasciculata cells as well. Injections of purified bovine growth hormone caused small but not significant increases in mitochondrial and smooth endoplasmic reticulum volumes. Growth hormone however did induce a significant increase in the surface area of mitochondrial membrane.

Adrenal Glands↗
PubMed1989

The kinetics of steroidogenesis activator polypeptide in the rat adrenal cortex. Effects of adrenocorticotropin, cyclic adenosine 3':5'-monophosphate, cycloheximide, and circadian rhythm.

The behavior of steroidogenesis activator polypeptide (SAP), a recently described modulator of cholesterol side-chain cleavage activity (Pedersen, R. C., and Brownie, A. C. (1987) Science 236, 188-190), was investigated in rat adrenocortical cells using a specific radioimmunoassay. In response to a maximal dose of adrenocorticotropic hormone (ACTH) (1 nM) or of 8-Br-cAMP (1 mM), an increase in intracellular SAP begins rapidly (less than 1 min) and reaches half-maximal and maximal levels (16-fold greater than basal) at 3 and 15 min, respectively. A plateau at this maximal concentration of SAP is then maintained. The levels of intracellular SAP content and of corticosterone output exhibit a similar dose-dependent response to ACTH (EC50 = 25 and 30 pM, respectively). Treatment of ACTH-stimulated cells with cycloheximide reverses the rise in SAP (t1/2 congruent to 5-7 min). In vivo the SAP content of adrenals from quiescent rats is concordant with the circadian rhythm of the pituitary-adrenal axis; at the apex (1800 h), adrenal SAP is 13-fold higher than at the nadir (0800 h), paralleling 2- and 7-fold variations in cholesterol side-chain cleavage activity and serum corticosterone levels, respectively. At both time points, SAP levels rise in response to stress. Of the rat tissues examined, only the major steroid-forming organs (adrenal cortex and gonads) had significant levels of immunoreactive, cAMP-responsive SAP, while cAMP-unresponsive immunoreactivity was also detectable in the thymus, spleen, and brain. Considered together with the biological activity previously demonstrated for SAP in vitro, these data are consistent with its role as a cAMP-dependent, cycloheximide-sensitive modulator of steroid biosynthesis.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1989

[Changes in the electrical activity of spinal cord neurons of adrenalectomized rats under the effect of adrenal cortex hormones].

Effect of dexamethasone and desoxycorticosterone on the electrical activity of neurons in dorsal and ventral horn of spinal cord evoked by sciatic nerve stimulation were studied in adrenalectomized rats as well as effect of the same hormones on the background activity of single cells in the dorsal horn. The results demonstrated that both hormones (dexamethasone and desoxycorticosterone) provided enhancement of the amplitude of the field potentials recorded from the dorsal half of the spinal cord and facilitation of the background neuronal discharges of the single cells under investigation. It was stated that gluco- and mineralocorticoid hormones exerted different effects on the activity of ventral horn neurons of the spinal cord: dexamethasone++ potentiated and desoxycorticosterone depressed the amplitudes of the field potentials recorded from the region of motoneurons. The presented data have shown the modulatory effects of neurosteroids on the electrical activity of the spinal cord neurons.

Adrenalectomy↗
PubMed1989

Steroid and xenobiotic effects on the adrenal cortex: mediation by oxidative and other mechanisms.

Because steroids reach high concentrations within the adrenal cortex, effects of the direct interaction of steroids and cytochrome P450 enzymes are possible and may involve oxidative damage. Steroid pseudosubstrate effects studied in cultured adrenocortical cells show that these effects are probably not mediated by steroid receptors. Release of oxidants during pseudosubstrate interaction with cytochrome P450s may be responsible for loss of enzymatic activity observed; enzyme activity can be protected by cytochrome P450 inhibitors, antioxidants, and lowered oxygen concentration. There may be pathological effects of pseudosubstrates in the adrenal cortex. Cytochrome P450/pseudosubstrate effects could be involved in the aging and death of adrenocortical cells in vivo, and necrosis of the adrenal cortex due to excessive ACTH stimulation or due to the action of adrenolytic chemicals could result from damage by oxygen radicals originating from cytochrome P450s. The possible mechanism of damage to the adrenal cortex by the xenobiotics dimethylbenzanthracene, TCDD, 3-methylcholanthrene, and o', p'-DDD are reviewed.

Adrenal Cortex↗
PubMed1976

Zonation of the adrenal cortex. II. Effect of BSA on coupling efficiency of mitochondria isolated from the zona glomerulosa of the bovine adrenal cortex.

Effect of bovine serum albumin on coupling efficiency of mitochondria isolated from the zona glomerulosa of the bovine adrenal cortex in various media was examined polarographically and electron microscopically. Albumin restored the coupling efficiency of mitochondria isolated from the zona glomerulosa regardless of isolation media when succinate or malate was oxidizable substrate. Respiratory controls greater than 5 were obtained. Albumin, however, had no effect when glutamate, beta-hydroxybutylate and pyruvate were the oxidizable substrates. The conditions have been found under which mitochondria of the zona glomerulosa stay in the orthodox configuration and yet coupled.

Adrenal Cortex↗
PubMed1978

Studies on cyclic nucleotides in the adrenal gland. VIII. Effects of angiotensin on adenosine 3',5'-monophosphate and steroidogenesis in the adrenal cortex.

Effects of angiotensin II on corticoid biogenesis and cAMP levels in the zona fasciculata-reticularis (the decapsulated fraction) and the zona glomerulosa (the capsular fraction) from the rat adrenal gland have been studied. Angiotensin II exclusively stimulated steroidogenesis in the zona glomerulosa without stimulation of the cAMP system, suggesting that steroidogenic action of this polypeptide does not involve the adenylate cyclase system. Angiotensin II was also found to stimulate cAMP-phosphodiesterase activity in the zona glomerulosa. An elevation of calcium concentration in the incubation medium has been observed to be effective in stimulating the production of aldosterone and cAMP by the capsular fraction. Angiotensin II caused a significant enhancement of the steroidogenic response of the capsular fraction to increasing calcium concentration regardless of the response of the cAMP system to calcium. This steroidogenic effect of angiotensin II was completely abolished by calcium antagonists added to the incubation medium without any inhibitory effect on the calcium-induced accumulation of tissue cAMP. These results suggest that angiotensin II acts on the adrenal II acts on the adrenal glomerulosa cell to increase intracellular calcium, which in turn directly stimulates steroidogenesis concomitant with the increased activity of phosphodiesterase.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1979

Studies on cyclic nucleotides in the adrenal gland. IX. Effects of ACTH on cyclic AMP and steroid production by the zona fasciculata-reticularis of the adrenal cortex.

Effects of ACTH and calcium on cyclic AMP and steroid production by the zona fasciculata-reticularis (the decapsulated fraction) from the rat adrenal cortex have been studied. Increasing concentrations of extracellular calcium enhanced the action of ACTH on cyclic AMP and steroid production. These effects of ACTH with calcium were prevented by lanthanum, but not by tetracaine or verapamil, suggesting that ACTH stimulation may be mediated by calcium through a process not involving the tetracaine- or verapamil-vulnerable step(s) of the calcium current. High concentrations of external calcium itself increased cyclic AMP accumulation without any increase in steroidogenesis. A calcium ionophore, X537A was stimulatory for steroidogenesis but inhibitory with respect to cyclic AMP accumulation. Considered together with the findings of AMP increase, these results suggest that ACTH primarily increases intracellular calcium mobilization thus stimulating directly the steroidogenesis, which is independent of the cyclic AMP system. Relatively high concentrations of ACTH activate the adenylate cyclase, which depends on extracellular calcium to increase cyclic AMP levels and stimulation of steroidogenesis by the decapsulated fractions of the adrenal cortex.

Adrenal Cortex↗
PubMed1979

Effects of ACTH and calcium on cyclic AMP production and steroid output by the zona glomerulosa of the adrenal cortex.

Effects of ACTH and calcium on cyclic AMP production and steroid output by the zona glomerulosa (the capsular fraction) from the rat adrenal cortex have been studied. Although high concentrations of extracellular calcium potentiated the stimulatory action of ACTH on cyclic AMP and aldosterone output, tetracaine or verapamil inhibited aldosterone output but not cyclic AMP production during ACTH-stimulation. Lanthanum reduced both aldosterone and cyclic AMP accumulation induced by ACTH. These results suggest that an extracellular calcium would be essential in stimulating the capsular steroidogenesis without involvement of the cyclic AMP system.

Adrenal Cortex↗
PubMed1986

Inhibition by adenosine of ACTH-stimulated adenylate cyclase and steroidogenesis in the adrenal cortex.

Effects of adenosine analogs on ACTH-stimulated adenylate cyclase activity and steroidogenesis in rat adrenocortical glands have been studied. Adenosine analogs inhibited ACTH-stimulated adenylate cyclase activity by a GTP-dependent process. Methylxanthines reversed the inhibitory effect of N6-phenyl-isopropyl-adenosine (PIA), but not of 2',5'-dideoxy-adenosine. These results suggest that adenosine negatively regulates the stimulation of adenylate cyclase by ACTH at the external and the internal site of the membrane. The inhibitory effect of PIA on ACTH-stimulated steroidogenesis by isolated cells was antagonized by methylxanthines. PIA also inhibited steroidogenesis induced by dibutyryl cAMP, suggesting an inhibitory action of the nucleoside distal to the cAMP system. These results suggest the presence of a common site located in the external membrane for adenosine which subsequently mediates two independent processes, one is negatively coupled to the adenylate cyclase and the other to steroidogenesis for negative feedback controls of the adrenal cortex.

1-Methyl-3-isobutylxanthine↗
PubMed1976

Plasma 16 beta-hydroxydehydroepiandrosterone in normal and pathological conditions in man.

Plasma 16beta-hydroxydehydroepiandrosterone (16 beta-OH-DHEA) levels in normal subjects and patients with certain pathological conditions have been evaluated using radioimmunoassay of the steroid. Plasma 16 beta-OH-DHEA levels in normal subjects rose sharply during adolescence and then declined slowly throughout adult life: 192 +/- 54 (SE) pg/ml between 7 and 11 yrs., 395 +/- 22 pg/ml between 15 and 19 yrs, 330 +/- 29 pg/ml between 20 and 39 yrs., 291 +/- 35 pg/ml between 40 and 59 yrs., and 124 +/- 20 over 60 yrs. No significant difference was found between male and female subjects. Plasma 16 beta-OH-DHEA rose significantly (P less than 0.001) during ACTH stimulation, declined significantly (P less than 0.005) during dexamethasone suppression, declined significantly (P less than 0.05) during gonadal suppression, rose significantly (P less than 0.05) during gonadal stimulation and rose significantly (P less than 0.005) after the administration of WIN 24,540, an inhibitor of 3 beta-ol-dehydrogenase. The concentration of 16 beta-OH-DHEA in adrenal venous blood was higher than in inferior vena cava blood, but 16 beta-OH-DHEA in hepatic venous blood was not higher than 16 beta-OH-DHEA in arterial blood. It is inferred that 16 beta-OH-DHEA is secreted directly by the adrenal cortex and probably the gonads. Plasma 16 beta-OH-DHEA was elevated in normal pregnant women, pregnant women with toxemia, and in patients with Cushing's disease, ectopic ACTH-producing tumor, and congenital adrenal hyperplasia, but it was not elevated in patients with low-renin essential hypertension.

Adolescent↗
PubMed1992

Disturbances in dexamethasone suppression test and lower availability of L-tryptophan and tyrosine in early puerperium and in women under contraceptive therapy.

This study investigates the function of the hypothalamic-pituitary-adrenal (HPA)-axis and the availability of L-tryptophan and tyrosine to the brain in postpartum women and in women taking long-term oral contraceptives. To this end, we have measured the following parameters in 50 women (i.e. 9 normal controls, 10 women taking oral contraceptives, and 31 postpartum females): plasma cortisol, L-tryptophan, tyrosine and the amino acids (CAA) known to compete with them for transport through the blood-brain barrier. We have determined the effects of 1 mg of dexamethasone on the above-mentioned biological markers in postpartum females. Plasma cortisol and tyrosine were significantly higher and lower, respectively, in puerperium and in women under contraceptive therapy as opposed to normal controls. L-Tryptophan was significantly lower in postpartum females, whilst the L-tryptophan/CAA ratio did not differ across the three study groups. Postpartum females revealed a significant negative relationship between the availability of L-tryptophan to the brain and postpartum mood, as measured by Zung's Depression and Anxiety Scales and State Anxiety Inventory. Dexamethasone had a significant suppressive effect on L-tryptophan/CAA and tyrosine/CAA ratios, with cortisol nonsuppression appearing in 82% of the postpartum females.

Adult↗
PubMed1978

The effect of oral contraceptive treatment on the serum concentration of dehydroisoandrosterone sulfate.

Dehydroisoandrosterone sulfate (DS), the major C19-steroid in the human circulation, was measured in serum obtained from blood samples collected daily (8 to 10 A.M.) throughout the menstrual cycles of eight normal, presumably ovulatory women and daily throughout the treatment cycles in four women taking an oral contraceptive (norethindrone, 1 mg., plus mestranol, 80 mcg.). The serum concentrations of DS in the ovulatory women ranged from 1,025 to 4,200 ng. per milliliter; mean, 2,062 +/- 137 ng. per milliliter (mean and standard error; n = 213). Serum DS concentrations during the follicular and luteal phases of the menstrual cycles of these women were similar. In women taking the oral contraceptive, the plasma DS concentrations ranged from 475 to 1,400 ng. per milliliter (mean, 895 +/- 83; n = 119). The 24 hour secretory pattern of DS was evaluated in one subject during a nontreatment cycle and again after 20 days of oral contraceptive treatment. In this subject, the mean serum DS level was 34 per cent lower during oral contraceptive treatment than the level before treatment. The decrease in the serum concentration of DS during oral contraceptive treatment likely results from a reduction in adrenal DS secretion since DS secretion by the normal human ovary is negligible and ovarian dehydroisoandrosterone secretion is small. Therefore, it is likely that the reduced serum DS levels in women taking oral contraceptives are the consequence of reduced adrenal secretion of DS resulting from reduced release of adrenocorticotropic hormone.

Adrenal Cortex↗
PubMed1979

Transitory hypoadrenalism due to long-term treatment with antiovulatory compounds.

A considerable number of women receiving antiovulatory compounds or estrogens complain of weakness and fatigability, suggesting a state of clinical hypoadrenalism. For this reason, levels of plasma ACTH and plasma cortisol were determined in 25 women with such complaints both during treatment and at various intervals after cessation of this treatment. The results obtained showed that there was a significant inhibition of ACTH secretion during long-term treatment with antiovulatory compounds or estrogens, and in half of the cases, there was a delay in normalization of the pituitary-adrenal axis following interruption of the drug, supporting a state of transitory hypoadrenalism.

Adrenal Insufficiency↗
PubMedDate not supplied

Toxaphene: accumulation in the adrenal cortex and effect on ACTH-stimulated corticosteroid synthesis in the rat.

Uptake and distribution of [14C]toxaphene was studied in the adrenals of rats using whole-body autoradiography. An accumulation of radioactivity was seen in the adrenal cortex (zona fasciculata) 1-24 h after a single gavage of [14C]toxaphene (16 mg/kg b.w.). In in vitro studies toxaphene was found to inhibit ACTH-stimulated corticosterone synthesis in the cultured rat adrenocortical cells (IC50 2.8 X 10(-5) M). Moderate but significant inhibition (P less than 0.001) of ACTH-stimulated corticosterone synthesis was also observed in the adrenocortical cells isolated from rats after a prolonged exposure (5 weeks) to low levels (1.2 ppm) of toxaphene in feed. The results indicate a direct adrenotoxic effect of toxaphene.

Adrenal Cortex↗