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PubMed1977

Aminergic and thermoregulatory mechanims in hypothalamic regulation of growth hormone in cats.

In conscious cats intravenous infusion of L-dopa (20 mg/kg) increased plasma growth hormone (GH), hydrocorticosterone (17-OHCS), and glucose while lowering midbrain (core) temperature (Tmb). Peripheral blockade of aromatic amino acid decarboxylase by L-alpha-hydrazino-methyldopa (MK 486) abolished only L-dopa hyperglycemia, indicating CNS stimulation by de novo catecholamines caused endocrine and temperature changes. Phenoxybenzamine but not pimozide pre-treatment abolished GH release after L-dopa. Apomorphine infusion alone did not alter basal GH. These data indicate central alpha-adrenergic mediation of GH release. Norepinephrine (NE) injected (5 or 10 microgram) into the preoptic anterior hypothalamus (POAH) (7 of 10 cases) and medial hypothalamus (17 of 30) raised GH while lowering Tmb, in agreement with alpha-adrenergic mediation. Responsive sites were distributed in ventral and dorsal medial hypothalamus and extended into the thalamus. Cooling of the POAH by implanted thermode raised GH in association with shivering, vasoconstriction, and rise in Tmb. Correlation between GH release and change in Tmb after L-dopa, central NE injection, and POAH cooling suggests hypothalamic integration of GH release with thermoregulation. Intravenous infusion of 5-hydroxytryptophan after MK 486 raised GH and 17-OHCS, suggesting serotonergic mechanisms also control GH and ACTH.

18-Hydroxycorticosterone↗
PubMed1976

Mineralocorticoid activity of 18-OH-DOC and DOCA in dogs with an aortic-caval fistula.

The mineralocorticoid activity of 18-hydroxydeoxycorticosterone (18-OH-DOC) was measured during chronic electrolyte balance studies or during the postprandial increase in electrolyte excretion in conscious dogs with an aortic-caval fistula. In the chronic balance study, daily doses of DOCA and 18-OH-DOC ranging from 1 to 25 mg were administered intramuscularly for 3 consecutive days each, 6 h prior to feeding. For the postprandial study, 2-10 mg of DOCA and 18-OH-DOC were administered at feeding and postprandial electrolyte excretion was measured hourly for 6 h. Sodium and fluid retention in the dogs with an aortic-caval fistula was related to the dose of mineralocorticoid administered and equivalent sodium-retaining responses were achieved with 6-10 times more 18-OH-DOC than DOCA. Rapid absorption of both steroids was suggested from the postprandial measurements of urinary sodium excretion. Slight potassium retention occurred during the chronic administration of large doses of DOCA but the postprandial potassium responses produced by the steroids were variable and suggested a slight kaliuresis. The data also emphasize the importance of mineralocorticoids in sodium retention and ascites formation in this experimental model of high-output heart failure.

18-Hydroxycorticosterone↗
PubMed1979

Fetal rat adrenal growth and steroidogenesis in vitro after maternal dexamethasone treatment.

Two groups of female rats were treated with dexamethasone phosphate (DEX) for 24 h. One group received DEX in drinking water (10 micrograms/ml) on the 15th day of pregnancy (DEX15--16), and the second group on the 17th day of pregnancy (DEX 17--18). The mothers and fetuses were sacrificed on the 20th and 22nd days of pregnancy. DEX reduced adrenal weights and concentration of corticosterone in plasma of the treated females and their fetuses. Fetal body weight was also reduced. However, the lightest adrenal glands were found in fetuses of the DEX17--18 mothers. Furthermore, the 19-day-old fetuses belonging to the DEX17--18 mothers had smallest amounts of corticosterone in plasma, and in plasma, and their adrenal glands produced the lowest amounts of radioactive corticosterone, 11-doxycorticosterone and 18-hydroxy-11-deoxycorticosterone from 4-14C progesterone after 1 h or incubation in vitro. In the 21-day-old fetuses belonging to both the groups of treated mothers, the production of steroids by the adrenal glands was similar and to the same extent reduced in comparison to the control fetuses.

18-Hydroxycorticosterone↗
PubMed1976

Mineralocorticoid secretion in essential hypertension with normal and low plasma renin activity.

In 19 control subjects, 33 patients with essential hypertension and normal plasma renin activity (PRA) and 11 patients with low PRA, secretory rates of 18-hydroxy-11-deoxy-corticosterone (18-OH DOC), 11-deoxycorticosterone (DOC) and corticosterone were measured. Patients with low PRA were significantly older and had higher arterial pressure and slightly lower plasma potassium levels than patients with normal PRA. Mean 18-OH DOC secretion rate was higher in patients with normal PRA (603 +/- 112 SEM mug/24 hr) than in control subjects (219 +/- 19) and considerably higher (P less than 0.001) in patients with low PRA (1800 +/- 472). DOC and corticosterone secretion rates were within normal limits in most hypertensive patients. Plasma aldosterone was significantly higher in the hypertensive population than in control subjects whereas no significant difference was observed between the low- and normal-renin groups. A significant (P less than 0.01) mutual positive correlation was found between the secretion rates of 18-OH DOC, DOC and corticosterone in patients with low plasma renin activity. In contrast, there was no correlation between the secretion rates of the three mineralocorticoids in control subjects and patients with normal plasma renin activity. These data suggest a biosynthetic variation of the mineralocorticoid pathways in essential hypertension.

18-Hydroxycorticosterone↗
PubMed1990

Investigations on the morphology and function of adrenocortical tissue regenerated from gland capsular fragments autotransplanted in the musculus gracilis of the rat.

This paper describes the function and morphology of regenerated adrenocortical nodules obtained by implanting, in the musculus gracilis of rats, several (n = 6-7) fragments of the capsular tissue of their excised adrenal glands. Four months after the operation, each bilaterally adrenalectomized rat developed six or seven well encapsulated adrenocortical nodules about 2-3 mm in diameter and always lacking chromaffin cells, and displayed almost complete normalization of basal and stimulated blood levels of corticosterone, but not of aldosterone. In vitro study showed that regenerated nodules were well functioning as far as glucocorticoid production was concerned. Accordingly, electron microscopy and stereology indicated that the majority of the parenchymal cells (independently of their location in the outer subcapsular, middle, or inner portions) closely resembled those of the zonae fasciculata/reticularis of the adrenal gland of age-matched sham-operated rats. By contrast, regenerated nodules evidenced a relative impairment in aldosterone secretion, and this was coupled with the presence of only a few zona glomerulosa-like cells. Such cells were grouped in small islets located near the few connective trabeculae detaching from the capsule, and autoradiography showed that they were the only parenchymal elements of the nodule able to bind [125I]angiotensin-II. The possibility is suggested that the paucity of zona glomerulosa-like cells in regenerated nodules could be ascribed to the absence of zona medullaris, which is currently thought to exert a paracrine control on the growth and secretion of zona glomerulosa in the rat adrenal glands.

18-Hydroxycorticosterone↗
PubMed1976

In vitro modification of rat adrenal zona fasciculata/reticularis function by the zona glomerulosa.

Following earlier findings, the possibility that the zona glomerulosa of the rat adrenal cortex may modify inner zone function was investigated. In a series of in vitro experiments designed to test this hypothesis it was found that: 1. Inner zone preparations gave significantly more steroid than either glomerulosa tissue incubated alone, or (for the first 40 min of a two hour incubation), an equivalent amount of whole adrenal tissue. Whole tissue yields were greater than glomerulosa alone only at the 120 min point. At no time did the whole tissue output approach the total anticipated by addition of separate inner zone and glomerulosa yields. 2. In 20 min incubations, inner zone steriod output generally could be depressed by the addition of a glomerulosa preincubation medium (PIM), or a steroid extract of a glomerulosa PIM, or by the addition of 100 ng aldosterone. Inner zone PIM had less effect. 3. Higher concentrations of aldosterone gave increased inhibition of inner zone corticosteroid production. The results indicated that only a part of the total corticosterone output was aldosterone sensitive in this way. 4. More specific analysis of the steroids showed that yields of corticosterone from endogenous precursors were depressed by aldosterone, but deoxycorticosterone and 18-hydroxydeoxycorticosterone were not. In the same incubations the presence of aldosterone had no effect on the formation of these three products from [3H]pregnenolone. In total the results suggest that the presence of the glomerulosa may affect inner zone function by inhibiting the secretion of corticosterone formed from endogenous precursors. It is possible that aldosterone is the agent of this effect.

18-Hydroxycorticosterone↗
PubMed1990

An antioxidant drug, silibinin, modulates steroid secretion in human pathological adrenocortical cells.

Because human adrenocortical cells from different adrenal disorders exhibit pathologically altered corticosteroid synthesis, and free radical mechanisms may induce pathological changes in the activities of corticosteroid biosynthetic enzymes (cytochrome P-450), we examined the effect of an antioxidant, silibinin, on basal and ACTH-stimulated secretion of several corticosteroids in isolated adrenal cells from an aldosterone-producing adenoma, atrophied adrenal tissues surrounding the adenoma, and hyperplastic adrenals from Cushing's syndrome. In the presence of a high concentration (100 mumol/l) of silibinin, variably diminished secretion of basal aldosterone, corticosterone, cortisol, 18-OH-corticosterone and 11-deoxycorticosterone was found. In contrast, the addition of 0.01 mumol silibinin/l, which failed to produce a clear effect on basal corticosteroid secretion, resulted in a potentiation of ACTH-stimulated secretion of several corticosteroids in the adenomatous and hyperplastic adrenocortical cells. These results suggest that the dose-dependent dual effect of silibinin on corticosteroid secretion may be attributed to corresponding changes in the activities of cytochrome P-450 enzymes, and that stimulation of ACTH-induced corticosteroidogenesis by silibinin is presumably due to the antioxidant property of the drug.

18-Hydroxycorticosterone↗
PubMed1991

Elevated 18-hydroxy-corticosterone in inbred salt-sensitive rats.

Rats susceptible to the hypertensive effect of dietary salt (SS/Jr) have excess 18-hydroxydeoxycorticosterone (18-OH-DOC) and 19-nor-DOC compared to control rats (SR/Jr). This may be caused by an abnormal adrenal 11 beta-hydroxylase, which catalyzes the 11 beta, 18, and 19-hydroxylations of DOC. A comparison of the urinary products of this enzyme including 18-OH-DOC, 19-nor-DOC, corticosterone (B), and 18-OH-B have not been described in the SS/Jr. Therefore, these steroid products were measured at 7 and 12 weeks of age in 36 weanling male and female, SS/Jr and SR/Jr (n = 9 in each group), on a low-salt diet. In both the male and female SS/Jr urinary free levels of 18-OH-DOC, 19-nor-DOC, and 18-OH-B were elevated, while B was not different at 6 and 10 weeks of age. The largest increases were in 18-OH-B levels, and these levels correlated with 18-OH-DOC and B but not 19-nor-DOC. The high degree of correlation between these steroids probably reflects their closely related dependence on adrenal 11 beta-hydroxylase biosynthesis.

18-Hydroxycorticosterone↗
PubMed1975

ACTH and growth hormone relationship in fetal rat adrenal steroidogenesis in vitro.

The effects of growth hormone and ACTH, alone or in combination, on fetal rat adrenal steroidogenesis in vitro were examined on the last day of intrauterine development. ACTH increased, while growth hormone did not affect fetal adrenal weight. ACTH increased fetal rat adrenal steroidogenesis, hydroxylation of 4-14C-progesterone to corticosterone, 18-hydroxy-11-deoxycorticosterone, 11-hydroxycorticosterone and aldosterone. Growth hormone alone had no effect on fetal adrenal steroidogenesis. ACTH and growth hormone administered together increased the conversion of progesterone to the above mentioned steroids to a greater extent than ACTH alone. The results indicate that growth hormone may participate in the fetal rat adrenal steroidogenesis potentiating the effects of fetal pituitary ACTH.

18-Hydroxycorticosterone↗
PubMed1991

Interference of C17-spirosteroids with late steps of aldosterone biosynthesis. Structure-activity studies.

Structure-activity relationships concerning the steroidal skeleton as well as the C21,17-ring systems could be established while investigating the inhibitory effects of 27 different C17-spirosteroids on aldosterone synthesis in vitro. 18-hydroxylation appeared to be the crucial point of interference with all active compounds, whereas impairment of 11 beta- and 21-hydroxylase, respectively, was of minor importance, i.e. occurring to a smaller degree and only with a few test substances. Inhibition of 18-hydroxylation was associated with the following structural features: C21,17-spiro-gamma-lactone ring with 17 beta-O-atom; 3-oxo group in combination with delta 4,5-6,7-diene structure or, alternately, combination of 3-oxo group or even a bulky 3-O-function, if it protrudes out of ring plane in beta-position, and 7a-thioalkyl- or thioacyl- or thiol groups; combination of 17-spiro-gamma-lactone and a 3-O-function may result in an active compound even without 7a-substituents, provided there are no additional groups fixed on the steroidal skeleton. Elimination of an angular methyl group (----nor-compound), however, is acceptable. On the other hand, inhibitory potency is abolished or diminished by the following structural features: 7a-groups containing oxidized sulphur (e.g. suphoxy- or sulphonyl groups); bulky 3-substituents fixed in the ring plane via double bond; 18-alkyl groups; 6 beta-substituents; 2-substituents in absence of 7a-groups, depending on their configuration (e.g. cycle or chain); introduction of a heteroatom at C21, i.e. instead of the carbonyl-C-atom. Mespirenone (CAS 87952-98-5), the test substance of central concern, possesses favourable structural features finding its expression in a correspondingly enhanced inhibitory action.

17-alpha-Hydroxyprogesterone↗
PubMedDate not supplied

[Effect of acid polysaccharides on the corticosteroid biosynthesis].

Repeated administration of carboxymethylchitin and chondroitinsulfate to rats in doses of 20 and 120 mg/kg/24 hours led to reduction (by 40-55%) of the rate of aldosterone and 18-oxycorticosterone biosynthesis by the rat adrenal glands in vitro. Carboxymethylcellulose, algin and hyaluronic acid displayed no inhibitory effect. In case of a single administration of carboxymethylchitin to rats (50 mg/kg) inhibition of the rate of aldosterone and 18-oxycorticosterone biosynthesis was seen 48 hours after the administration of the preparation and lasted four days. No inhibitory effect was induced by the addition of 10 mg/kg of acid polysaccharides into the incubation medium of the adrenal glands.

18-Hydroxycorticosterone↗