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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↗
PubMed1981

[Effect of splenin and its fractions on the functional state of the adrenal cortex].

Effect of splenin (1 ml) and its fractions (0.5 ml) on adrenocortical function was studied after a single intramuscular injection of the preparations into rats. Splenin and its fractions containing water-soluble substances reduced the content of ascorbic acid in the rat adrenals thereby indicating the increased synthesis of adrenocortical hormones. Adenosine-5-monophosphate is one of the basic biological substances contained by splenin and its water-soluble fractions. It produces a stimulant effect on the synthesis of adrenocortical hormones.

Adenosine Monophosphate↗
PubMed1980

Studies on cyclic nucleotides in the adrenal gland. X. Effects of adrenocorticotropin and prostaglandin on adenylate cyclase activity in the adrenal cortex.

Effects of ACTH and prostaglandin E1 (PGE1) on adenylate cyclase activities in the zona glomerulosa (the capsular fraction) and the zona fasciculata-reticularis (the decapsulated fraction) from rat adrenocortical glands have been studied. Stimulation by ACTH of adenylate cyclase activity was observed in both the capsular and decapsulated fractions in a similar dose-dependent manner. PGE1 only stimulated adenylate cyclase activity in the capsular fraction. The maximal stimulations induced by ACTH and PGE1 were additive on the capsular enzyme. A prostaglandin antagonist, polyphloretin phosphate failed to inhibit ACTH stimulation of adenylate cyclase at a concentration which completely blocked the effect of PGE1. [3H]PGE1 bound to subcellular fractions of both the capsular and decapsulated fractions of the gland. These results suggest that the capsular fraction possesses receptors for PGE1 coupled to the adenylate cyclase system which are distinct from those for ACTH. On the other hand, PGE1 receptors in the decapsulated fraction seem not to be coupled to the adenylate cyclase system.

Adenylyl Cyclases↗
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↗
PubMed1984

Disorders of the adrenal cortex: their effects on electrolyte metabolism.

The adrenal cortex is an important factor in the control of electrolyte and water balance and in blood pressure homeostasis. Not surprisingly, therefore, hyper- and hyposecretion of one or more of its products has extensive repercussions. Hypersecretion of aldosterone, as seen in primary hyperaldosteronism and related diseases, and of other mineralocorticoids such as corticosterone and/or 11-deoxycorticosterone, as seen in 17 alpha-hydroxylase deficiency or 11 beta-hydroxylase deficiency syndromes, respectively, are associated with hypertension, sodium retention, potassium wastage and a metabolic alkalosis. On the other hand, impaired secretion, as in Addison's disease or in congenital deficiencies of other steroid-synthesizing enzymes, leads to hypotension, sodium loss with hypovolaemia, and hyperkalaemia. In each case, these disturbances of electrolyte metabolism may cause neurological and muscle dysfunction. The relationship between glucocorticoid hypertension and electrolyte metabolism is less clear and the importance of the adrenal cortex in the aetiology of essential hypertension is still being assessed.

Addison Disease↗
PubMed1985

Estradiol and melatonin effects on adrenal cortex of ovariectomized and pinealectomized rats.

Studies on the effect of pinealectomy (PX) and melatonin on adrenal cortex of ovariectomized and estradiol replaced rats were performed. Neither PX nor melatonin replacement changed corticosterone output by adrenal homogenate, 11 beta-hydroxylase activity, liver corticosterone metabolism or serum corticosterone level, however, melatonin increased adrenal 5 alpha-reductase activity. On the other hand, PX of 14 months duration resulted in an increase in intraadrenal 5 alpha-reductase activity. PX did not modify estradiol effect on rat adrenal cortex, while concomitant estradiol-melatonin administration increased corticosterone output by adrenal homogenate. Stimulatory effect of estradiol on liver corticosterone metabolism was observed only in the presence of pineal gland or exogenous melatonin. In non of experiments, 45 nmole/ml of melatonin added into incubation medium stimulated adrenal 5 alpha-reductase activity. Obtained results cast doubt on a physiological role of melatonin in regulation of adrenocortical secretory activity in ovariectomized rats and suggest that estradiol effect on the adrenal cortex is not mediated by the pineal gland.

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↗
PubMed1980

Progesterone effects on adrenal cortex of intact and ovariectomized rat.

Studies on the effects of progesterone on rat adrenal cortex were performed on two age groups of intact or ovariectomized female rats. Ovariectomy was performed on animals weighing 150-170 g and autopsies were carried out 6 weeks and 8.5 months after surgery (4- and 11-month-old animals). 12 days before autopsy part of the animals were treated with progesterone at a daily dose of 5 mg per rat, the others received a single injection of depot-estradiol or jointly with progesterone and estradiol. Intact female rats of a corresponding age were treated with progesterone or vehicle only. In younger intact female rats progesterone lowers the relative adrenal weight and corticosterone output by whole adrenal homogenates. In older rats despite the lowering in absolute and relative adrenal weights there were no changes in corticosterone output. In ovariectomized rats of both age groups progesterone had no marked effects on studied parameters while estradiol resulted in an increase in adrenal weights and corticosterone output. Part of the changes evoked by estradiol were prevented by concomitant progesterone administration. The above described changes were accompanied by morphologic alterations. Performed studies show that progesterone effects on the rat adrenal cortex are modified by the ovaries and depend on the age of animals.

Adrenal Cortex↗