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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

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↗
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↗
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↗