PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “18-Hydroxycorticosterone”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1979

[In vivo and in vitro studies on 18-hydroxy-11-deoxycorticosterone and 18-hydroxycorticosterone in normal subjects and in those with various adrenocortical disorders (author's transl)].

Simultaneous measurement of 18-hydroxy-11-deoxycorticosterone (18-OH-DOC) and 18-hydroxycorticosterone (18-OH-B) in the peripheral plasma was carried out on normal subjects and in patients with adrenocortical disorders. The mean plasma levels of 18-OH-DOC at 0800h in normal males and in the follicular and luteal phases of normal females were 8.2 +/- 3.9 ng/100 ml (Mean +/- SD), 7.8 +/- 2.6 ng/100ml and 11.5 +/- 2.8 ng/100ml, respectively. The corresponding levels of 18-OH-B in normal males and in the follicular and luteal phases of normal females were 10.3 +/- 4.2 ng/100ml, 12.4 +/- 4.5 ng/100ml and 13.8 +/- 4.1 ng/100ml, respectively. No differences between the sexes nor the phases of the menstrual cycle were confirmed. ACTH stimulation increased plasma concentrations of 18-OH-DOC and 18-OH-B by 5.1 and 4.4 times respectively, while dexamethasone markedly decreased these 2 steroids. An upright posture increased these steroids significantly. In patients with Cushing syndrome, plasma levels of these 2 steroids were rarely high in cases with adrenocortical hyperplasia and adrenocortical carcinoma, while they were usually within the normal range in adrenocortical adenoma. These 2 steroid levels were increased in primary aldosteronism, idiopathic hyperaldosteronism and congenital 17 alpha-hydroxylase deficiency. They were decreased in Addison's disease and the salt-loosing type of congenital 21 alpha-hydroxylase deficiency. Patients with congenital 21 alpha-hydroxylase deficiency (simple form) showed elevated levels of 18-OH-DOC and normal levels of 18-OH-B. In vitro production of 18-OH-DOC and 18-OH-B was studied by tissue slices of the normal adrenal cortex, adrenocortical carcinoma causing Cushing syndrome, aldosteronoma and nodular hyperplasia with hyperaldosteronism. In the normal adrenal cortex, the mean production rates of 18-OH-DOC and 18-OH-B were 31 and 26 ng/g tissue/hr, respectively. ACTH and angiotensin II significantly increased the production of both 18-OH-DOC and 18-OH-B. In adrenocortical carcinoma, the production of these steroids was markedly diminished and not stimulated with either ACTH or angiotensin II. Aldosteronoma tissue produced these 2 steroids 20 to 40 times that of the normal adrenal tissue and was significantly increased with the addition of ACTH and angiotensin II. Nodular hyperplasia with hyperaldosteronism produced much 18-OH-DOC and 18-OH-B, but did not respond to ACTH and angiotensin II.

18-Hydroxycorticosterone↗
PubMed1979

[Cytochrome P-450 and transformation from 18-hydroxycorticosterone to aldosterone].

The authors have studied the in vitro conversion of 18 hydroxycorticostérone to aldosterone (18 oxidation) by duck adrenal subcellular fractions. Considering the new hypothesis about the mechanism of this step (hydroxylation mechanism) the authors have investigated a possible relationship between this reaction and cytochrome P450. With experimental conditions described, data show that metyrapone, a cytochrome P450 competitive inhibitor does not inhibit 18 oxidation. In contrast, 18 oxidation is inhibited by spirolactones (spironolactones, canrenone, potassium canrenoate). These compounds act at the cytochrome P450 level but have also an uncoupling effect which has been recently discovered. The effects of metyrapone and spirolactones on 18 oxidation as well as the different behaviour between biologicaly and organically synthetised 18 hydroxycorticosterone allow us to propose hypotheses for the mechanism of this step.

18-Hydroxycorticosterone↗
PubMed1979

Assay and properties of 18-hydroxylation of endogenous and exogenous corticosterone in rat adrenals. Evidence for heterogeneity of 18-hydroxylase activity.

A mass fragmentographic technique for assay of 18-hydroxylation of labeled (exogenous) and unlabeled (endogenous) corticosterone in adrenal mitochondria and in reconstituted cytochrome P-450 systems has been developed. An extract of an incubation of [14-14C]corticosterone is subjected both to thin-layer radiochromatography and to mass fragmentography (as O-methyloxime-trimethylsilyl ether derivative). In the latter procedure the ions at m/e 605 and 607 (specific for the derivatives of unlabeled and labeled 18-hydroxycorticosterone, respectively), at m/e 591 and 593 (specific for the derivatives of unlabeled labeled aldosterone, respectively) and at m/e 548 and 550 (specific for the derivatives of unlabeled and labeled corticosterone, respectively) were followed through the gas-liquid chromatography. From the ratio between the peaks obtained in the mass fragmentography and from the percentage conversion of [4-14C]corticosterone obtained in the thin-layer radiochromatography, the amount of endogenous and exogenous 18-hydroxycorticosterone and aldosterone could be calculated. The effects of time, enzyme, and substrate concentration of 18-hydroxylation were studied and optimal conditions for assay were determined. Under most conditions, the ratio between labeled and unlabeled 18-hydroxylated products was about constant, indicating that labeled and unlabeled corticosterone were not in equilibrium. It was ascertained that the 18-hydroxycorticosterone and aldosterone formed in the incubations were derived from corticosterone. [4-14C]18-Hydroxydeoxycorticosterone was not converted into aldosterone or 18-hydroxycorticosterone. In vitro studies with different 18-hydroxylase inhibitors (spironolactone, canrenone, and canrenoate-K) and studies with rats pretreated with KCl in drinking fluid suggest that 18-hydroxylation of corticosterone is catalyzed by an enzyme system different from that catalyzing 18-hydroxylation of deoxycorticosterone.

Adrenal Glands↗
PubMed1979

17 alpha-Hydroxylase deficiency. A combination of hydroxylation defect and reversible blockade in aldosterone biosynthesis.

We have studied the hormonal secretion and excretion patterns in a patient with the XX type of 17 alpha-hydroxylase deficiency. In the untreated state, the patient's urine contained only those steroids which do not require 17-hydroxylation in their biosynthesis. Aldosterone was not produced in the patient and the metabolic product of its immediate precursor, 18-hydroxy-11-dehydro-tetrahydrocorticosterone, was excreted in markedly elevated amounts. This apparent complete block in 18 oxidation was reversible upon long-term ACTH suppression within 27 days. Direct in vitro incubation of the patient's adrenal gland removed at operation demonstrated, 1) the complete lack of 17 alpha-hydroxylase activity, 2) the functional block in the ability to oxidize the hydroxyl group at the 18 methyl side chain. The addition of physiological concentrations of angiotensin to the incubation medium further showed, 3) angiotensin mildly stimulated the entire aldosterone biosynthetic pathway, 4) angiotensin directly stimulated the conversion of 18-hydroxycorticosterone to aldosterone. We propose that in this patient, 17-hydroxylase deficiency produced a decreased plasma concentration of cortisol, followed by stimulation of deoxycorticosterone production by ACTH. The resultant increase in extracellular fluid volume suppressed plasma renin activity. This resulted in a low plasma concentration of angiotensin II which directly suppressed oxidation of 18-hydroxycorticosterone to aldosterone. This defect has been called corticosterone methyl oxidase defect type 2.

18-Hydroxycorticosterone↗
PubMed1976

The influence of streptozotocin diabetes on adrenal function in male rats.

Male Wistar rats were treated with an i.v. dose of 100 mg/kg of Streptozotocin (STZ). Either 5 days or 1, 2 or 3 months after induction of diabetes, the adrenal function of these animals was studied. Short course diabetes (5 days) was accompanied by adrenal hypertrophy and high plasma corticosterone levels; during later periods the diabetic rats consistenly showed signs of adrenal hyperactivity, yet both adrenal weight and plasma corticosterone tended to be lower than in the 5 day-treated animals. Adrenal incubations with 14C-progesterone showed that 5 days and one month diabetic animals synthesized more deoxycorticosterone than controls; production of corticosterone and 18-hydroxydeoxycorticosterone was normal at all time periods studied. Synthesis of 18-hydroxycorticosterone, a compound which affects sodium metabolism, was increased in 5 day-treated rats; thereafter, the function of the zona glomerulosa seemed to be impaired in diabetic rats. These results suggest that early after induction of diabetes there is adrenal hyperfunction of the mixed type (i.e. gluco and mineralcorticoid), and that in the later periods (2-3 months), the deranged metabolism of the diabetic rat acts as a chronic stress.

Adrenal Glands↗
PubMed1978

Suppression of aldosterone biosynthesis by treatment of rats with adrenocorticotropin: comparison with glucocorticoid effects.

The treatment of rats with a high dose of ACTH resulted within 4 days in a marked suppression of aldosterone and deoxycorticosterone outputs by capsular adrenal tissue ("zona glomerulosa") incubated with and without serotonin and in decreased conversions of tritiated corticosterone and deoxycorticosterone to aldosterone and 18-hydroxycorticosterone, but in strikingly increased capsular adrenal conversions of tritiated deoxycorticosterone to corticosterone and 18-hydroxy deoxycorticosterone. ACTH also suppressed aldosterone biosynthesis in rats kept on a sodium-deficient diet. Corticosterone or dexamethasone, when added to the drinking fluid for 2 weeks, induced only small decreases in aldosterone biosynthesis from endogenous or exogenous precursors. Moreover, they significantly decreased the capsular adrenal conversion of added deoxycorticosterone to corticosterone and 18-hydroxydeoxycorticosterone. These results indicate that during prolonged ACTH treatment, the zona glomerulosa cell may be converted to a functional zona fasciculata type of cell. High levels of circulating mineralocorticoids and glucocorticoids seem to be minor contributory factors in the long term suppression of aldosterone biosynthesis by ACTH.

Adrenal Glands↗
PubMed1977

Metabolic responses to the administration of angiotensin II, K and ACTH in two salt-wasting syndromes.

Metabolic responses to the administration of Angiotensin II, K and ACTH are described in two salt-wasting syndromes: hypoaldosteronism in Jews from Iran, which is characterized by an enzymic block in the conversion of 18-hydroxycorticosterone to aldosteron; and pseudohypoaldosteronism, a disorder in which aldosterone secretion is high in association with renal tubular unresponsiveness to mineralocorticoids. The response of plasma and urinary aldosterone to K and ACTH is qualitatively normal in hypoaldosteronism; however, infusion of Angiotensin II, in a dose that was pressor and elevated aldosterone levels threefold in control subjects, was only pressor in hypoaldosteronism. In pseudohypoaldosteronism, plasma and urinary aldosterone respond to Angiotensin II, K and ACTH, notwithstanding very high basal hormonal levels.

Adrenocorticotropic Hormone↗
PubMed1978

The effect of chronic ACTH treatment on blood pressure and urinary excretion of steroids in the rat.

The effects of subcutaneous injections of synthetic ACTH during 14 subsequent days has been studied in the rat. ACTH caused a loss in body weight which was related to a negative water balance. Blood pressure rose rapidly and reached values higher than 180 mm Hg in all rats after 10 days of ACTH administration. During this period, urinary excretion of corticosterone and 18-hydroxy-deoxycorticosterone (18-OH-DOC) was increased more than ten times, while aldosterone excretion was increased only during the first two days. After withdrawal of ACTH, excretion of steroids normalized, or in some cases was even suppressed and water balance and body weight gain returned to normal values. However, blood pressure remained slightly higher than in controls after ten days. The effects of ACTH on water balance and blood pressure resemble those of corticosterone in the rat. The rapidly induced and sustained changes in blood pressure by ACTH administration suggest that this may be an useful model of experimental hypertension.

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↗