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At least 19 recordsLinked to original sources
PubMed1979

Desoxycorticosterone in normal pregnancy. II. Cortisol-dependent fluctuations in free plasma desoxycorticosterone.

Desoxycorticosterone (DOC) secretion increases during pregnancy. Administration of adrenocorticotropic hormone (ACTH) to women during the third trimester of pregnancy was noted previously to result in marked sodium retention, while aldosterone excretion declined. Since urinary tetrahydrodesoxycorticosterone increased substantially, sodium retention resulting from ACTH was ascribed to enhanced DOC secretion. Surprisingly, the elevated plasma DOC in late pregnancy failed to respond consistently to ACTH. Effects of ACTH upon total plasma concentrations and free indexes of DOC and cortisol were studied in pregnant women in the third trimester. As a result of ACTH, plasma cortisol and the free cortisol index increased strikingly; the plasma free DOC index rose markedly in those subjects in whom the total plasma DOC level was not altered appreciably and was unchanged or even increased slightly in the few subjects in whom the total DOC level decreased. The results support the proposition that the plasma free DOC fraction is increased because of displacement from corticosteroid-binding globulin by the ACTH-induced increment in cortisol. Resultant elevations of free DOC would not be evident from customary measurements of the total DOC concentration but, nonetheless, could contribute to sodium retention and also would be available for hepatic metabolism.

Adolescent↗
PubMed1978

Desoxycorticosterone in normal pregnancy. I. Sequential studies of the secretory patterns of desoxycorticosterone, aldosterone, and cortisol.

Plasma concentrations of desoxycorticosterone (DOC) and aldosterone are markedly elevated in pregnancy. Although DOC secretion in nongravid women has been assumed to be dependent mainly on adrenocorticotropic hormone (ACTH), in a previous study of women in the third trimester of pregnancy it was found to be unresponsive to ACTH, dexamethasone, and variations in salt intake. In this study plasma DOC, aldosterone, and cortisol levels, as well as their responses to ACTH stimulation and overnight dexamethasone suppression, were observed sequentially in seven normal women during the course of pregnancy and at three months post partum. Plasma DOC, aldosterone, and cortisol levels rose substantially during gestation, but increments in DOC did not necessarily coincide with those of the other two. Responses of all three corticosteroids to ACTH were enhanced during the first two trimesters compared to the nongravid state; DOC became unresponsive in the third trimester, while aldosterone and cortisol rose to an even greater extent. Elevated maternal DOC was not decreased significantly by dexamethasone at any stage of pregnancy, while plasma cortisol was suppressed. Nonsuppressibility of DOC with dexamethasone and also the lack of correlation of the rise in DOC with the increase in cortisol during the course of pregnancy suggest that increased DOC secretion in pregnancy does not arise from ACTH-dependent pathways of the maternal adrenal. The loss of responsiveness of DOC to ACTH in the third trimester suggests that the maternal adrenals have undergone an alteration in their steroidogenic response to ACTH, but also may indicate that their output of DOC has reached a maximal rate.

Adrenocorticotropic Hormone↗
PubMed1979

Liquid chromatographic determination of desoxycorticosterone acetate in oil injections.

To determine desoxycorticosterone acetate in oil injections, reverse phase partition chromatography on silanized, purified siliceous earth was used to separate the corticosteroid ester from the bulk of the oil vehicle. The latter was retained on the column while the steroid and the sterol and triterpenoid fractions of the oil were eluted. An internal standard was added to this eluate, which was then subjected to reverse phase high performance liquid chromatography (HPLC). The desoxycorticosterone acetate was quantitatively separated in the HPLC procedure from any free desoxycorticosterone, preservatives, and minor components of the oil. The suitability of the HPLC procedure was verified with a number of C18 packing materials, both pellicular and microparticular. The desoxycorticosterone acetate was adequately resolved from the internal standard, progesterone, with most C18 packing materials evaluated. The proposed procedure provides a suitable stability-indicating assay for desoxycorticosterone acetate in oil injections.

Chromatography, High Pressure Liquid↗
PubMed1979

[Influence of desoxycorticosterone on the reaction of isolated segments of coronary arteries to noradrenaline in the presence of pyrogallol].

The effect of the desoxycorticosterone on the noradrenaline-induced relaxation of coronary arteries waw studied in vitro, after a known inhibitor of COMT, pyrogallol. Relaxation induced by noradrenaline was enhanced by desoxycorticosterone. Relaxation in response to noradrenaline was increased by desoxycorticosterone. Pyrogallol potentiated the responses of coronary strips to noradrenaline and also reduced or abolished the enhancing effects of desoxycorticosterone. It is concluded that desoxycorticosterone enhances the reponse of coronary smooth muscle to noradrenaline by inhibiting and enzymatic pathway for the inactivation of catecolamines.

Animals↗
PubMed1975

Effects of triamcinolone and of desoxycorticosterone on renal function in sheep.

Sheep were treated for 10 or 17 days with triamcinolone acetonide, 0.1 mg/kg body weight/day, or desoxycorticosterone acetate, 0.1 mg/kg body weight/day, and the results of renal function studies during hydropenia and mannitol diuresis were compared with respective control periods. GFR was increased and urine concentration was unimpaired by treatment with triamcinolone. A consistent decrease in mannitol-induced Na excretion was observed, but with large variations in the mean change, in triamcinolone treatment periods. Treatment with desoxycorticosterone resulted in an increased GFR but with impaired urine concentrating capacity. The hypokalemia produced by desoxycorticosterone was not accompanied by an increase in urinary K excretion. During mannitol diuresis in sheep treated with desoxycorticosterone, there was a significant decrease in Na excretion when compared with control periods.

Animals↗
PubMed1977

Effects of dexamethasone, desoxycorticosterone, and ACTH on serum concentrations of thyroxine, 3,5,3'-triiodothyronine and 3,3',5'-triiodothyronine.

The effects of a pure glucocorticoid, dexamethasone, and a pure mineralocorticoid, desoxycorticosterone, on the serum concentrations of thyroxine (T4), 3,5,3'-triiodothyronine (T3), and 3,3',5'-triiodothyronine (reverse T3, rT3) were compared both in healthy subjects and in athyreotic T4-substituted patients. In addition, the effect of exogenous ACTH was examined in healthy subjects. Both in healthy subjects and in T4-substituted athyreotic patients, administration of a single oral dose of dexamethasone caused a rapid and sharp decrease in the serum concentration of T3, and a corresponding increase in the serum concentration of rT3. The T4 concentration was not changed. A single oral dose of desoxycorticosterone evoked no significant changes in the serum concentrations of T3, rT3, or T4 either in healthy subjects or in T4-substituted athyreotic patients. Like dexamethasone, ACTH (two i.v. injections of 60 IU each, at a 6-hour interval) evoked a serum T3 reduction and a serum rT3 increase. Hence, it appears that both endogenous and exogenous glucocorticoids, but not mineralocorticoids, may partially divert the deiodination of T4 from the activating (T4 lead to T3) to the inactivating (T4 leads to rT3) pathway.

Adrenal Cortex Hormones↗
PubMed1975

[Certain changes in the water-electrolyte metabolism in desoxycorticosterone acetate salt hypertension in rats adapted to high altitude hypoxia].

In the course of the development of desoxycorticosterone-acetate-salt hypertension the animals were noted to display high appetite of sodium chloride, a considerable increase of the weight of the heart, kidneys and adrenal glands, of the diameter of the glomeruli and the surface of the cortical and medullar zones of the kidneys, a decrease of the sodium and potassium gradient in the renal tissue. Adaptation to hypoxy is noted so cause a decrease in the interventricular factor, in the width of the glomerular zone of the adrenal glands, in the sodium concentration in the erythrocytes, an increase in the mass of the medullar layer of the kidneys, and an increase in the sodium and potassium gradients. When adaptation to hypoxy is combined with the effect of desoxycorticosterone-acetate-salt, hypertension develops to a lower degree than in non-adapted animals.

Adaptation, Physiological↗
PubMed1976

Is vasopressin involved in the pathogenesis of malignant desoxycorticosterone hypertension in rats?

Rats with unilateral nephrectomy were offered 1% sodium chloride as drinking fluid and were injected with desoxycorticosterone trimethylacetate (D.O.C.-T.M.A.) at weekly intervals. During the fourth to seventh week after the start of the experiment, malignant hypertension developed in most of the animals: body weight fell, reflecting volume depletion; serum osmolality and serum sodium and urea concentrations increased; in the kidneys malignant nephrosclerosis occurred. In such animals, plasma concentrations of arginine-vasopressin were increased ten-fold in comparison with control animals; intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood-pressure (B.P.) to normal or subnormal levels, while the injection of an angiotensin-I or angiotensin-II antibody did not affect B.P. In control animals none of the antibodies had an effect on B.P. It is concluded that in the pathogenesis of malignant D.O.C. hypertension vasopressin plays a role similar to that of renin-angiotensin in malignant renal hypertension.

Angiotensin II↗
PubMed1979

In vitro effects of desoxycorticosterone on vascular smooth muscle.

We present evidence in accord with the observations of S. Kalsner (Br. J. Pharmacol. 36: 582-593, 1969) that in the rabbit aorta, desoxycorticosterone (DOC) potentiates the contractile response to certain catecholamines by inhibiting their degradation by catechol-O-methyltransferase. In contrast, DOC depresses the contractile responses in rat aorta and tail arteries. To elucidate the mechanism of this depression the effect of DOC was evaluated under various conditions. DOC depressed the contractile response to epinephrine, phenylephrine, KCl, and angiotensin II. The depression was unaltered by ouabain or by a potassium-free solution, indicating that DOC did not produce its depression by altering Na-K-ATPase activity. The depression is unaltered in a chloride-free solution, demonstrating that the DOC effect is not caused by a change in membrane permeability to chloride. Radioisotope studies demonstrate that DOC does not alter membrane permeability to potassium. Removal of extracellular calcium with EGTA (ethylene glycol-bis (beta-aminoethyl ether) N, N'-tetraacetic acid) significantly reduced the magnitude of the DOC depression. Indirect evidence is presented suggesting that DOC might increase calcium binding to the plasma membrane, resulting in its stabilization and hence in a depression of the contractile response.

Angiotensin II↗
PubMed1977

Effect of some substituted pyrimidines on development of desoxycorticosterone-induced hypertension in rats.

Chronic (15-week) dietary administration of 2-thio-6-aminouracil (TAU, 1.0 and 2.0 g/kg food) provided significant protection against elevation of blood pressure and cardiac hypertrophy in male rats treated with desoxycorticosterone trimethylacetate (DTMA) (5.0 mg twice weekly for 10 weeks). Assessment of thyroid activity was made by measurement of 24 h 131I uptake by the thyroid gland, PBI concentration of serum, rate of oxygen consumption, hematocrit ratio, hemoglobin concentration, and thyroid weight. By all these criteria, the rats given either dose of TAU were hypothyroid. In contrast chronic (17-week) dietary administration of 5-carboxy-2-thiouracil (0.50 and 1.00 g/kg food) and 5-carboxy-4-hydroxy-2-thiouracil (2.00 g/kg food) provided minimal protection against elevation of blood pressure and cardiac hypertrophy in male DTMA-treated rats. These compounds appeared to possess little or no antithyroid activity at the doses used. The results suggest a rough correlation between the degree of hypothyroidism produced by the compounds and their effectiveness in preventing rise of blood pressure in DTMA-treated rats.

Animals↗
PubMed1979

Effect of chronic treatment with desoxycorticosterone on the dipsogenic response of rats to isoproterenol and angiotensin.

Administration of desoxycorticosterone (DOC) at a dose of 0.5 mg/kg/day to male rats for 6 weeks attenuated significantly the drinking response to acute subcutaneous administration of 5, 10 and 20 microgram isoproterenol/kg body weight. Chronic administration of DOC did not prevent the drinking response to acute intraperitoneal administration of angiotensin II (200 microgram/kg body weight). In contrast, the drinking response was enhanced compared with that of control rats given angiotensin II acutely. While attenuation of the drinking response to isoproterenol in DOC-treated rats may be attributed to depletion of renin from their kidneys, the mechanisms responsible for the enhanced drinking response to angiotensin II are not clearly understood.

Angiotensin II↗
PubMed1977

Studies in the biotransformation of cortisol to cortoic acids in man. III. 21-Oxidation of 4-14C,21-3H-desoxycorticosterone.

The metabolism of (4-14C, 21-3H) desoxycorticosterone (DOC) in man has been studied. DOC, like cortisol, undergoes oxidation at C-21 with the formation of acidic metabolites (2.3-8.2% of the dose). The release of 3H into the body water, either by oxidation or exchange, is approximately twice as great as the actual formation of acidic metabolites (as judged from the recovery of 14C in the urinary acidic fraction), but both parameters were considerably smaller than the corresponding values for cortisol. The principal metabolite isolated from the urine was 21-hydroxypregnanolone, which had an isotope ratio (3H/14C) greater than that of the dose; the pregnanetriols, which were formed in lesser amounts, had significantly lower isotope ratios than the dose. The absence of the 17-hydroxy group in DOC appears to modify C-21 oxidation, decreasing its magnitude and altering the character of the products.

Biotransformation↗
PubMed1978

Urinary free 18-hydroxy-11-desoxycorticosterone excretion in normal and hypertensive patients.

One hundred fourteen hypertensives and 20 normal controls were examined using a new clinical technique of measuring 24-h urinary free 18-hydroxy-11-desoxycorticosterone (18-OH-DOC) excretion in response to dietary salt manipulations and ACTH injections. The object was to avoid potential errors of random plasma sampling. Mean urinary free 18-OH-DOC in normals on 110 milliequivalent sodium diet was 1.84 +/- 0.69 microgram (mean +/- SD) and represented about 2% of the daily secretion rate of this steroid. Both in normals and hypertensives, urinary free 18-OH-DOC approximately doubled on low salt (P less than 0.01 for each) and rose about 10 times in response to ACTH injection (P less than 0.05 and P less than 0.01, respectively). Plasma and urinary free 18-OH-DOC showed good correlation in patients with essential hypertension on a low salt diet (r = 0.45, P less than 0.01). Suppressed renin patients showed no propensity toward excess 18-OH-DOC excretion and hypertensives with elevated 18-OH-DOC could not be distinguished by their aldosterone levels, cortisol levels, nor their responses to various stimuli. These data suggest 18-OH-DOC is predominantly secreted under ACTH control and, to a smaller extent, in response to salt changes. Hypertension characterized by chronic overproduction of 18-OH-DOC forms only a small percentage of the hypertensive population. It is proposed that measuring 24-h urinary free 18-OH-DOC excretion may be the best method of assessing its rate of secretion without resorting to injection of radiolabeled material.

18-Hydroxydesoxycorticosterone↗
PubMedDate not supplied

[A change in interneuronal transmission of excitation in the diencephalic regions of the brain under the influence of desoxycorticosterone].

Experiments were conducted on cats with the aid of electrophysiological methods and the use of blockers of cholino- and adrenoreceptors. It was shown that desoxycorticosterone facilitated the interneuronal transmission of excitation in the diencephalic portions of the brain. This was associated with the excitation under the effect of hormone of M-cholino- and beta-adrenoreceptors of the mediodorsal nucleus of the thalamus present on the postsynaptic membrane.

Animals↗
PubMed1978

Increase in urinary excretion of phosphates, hydroxyproline, and cAMP during acetate desoxycorticosterone + saline treatment in the rat.

We investigated the urinary excretion of phosphates, hydroxyproline, and cAMP in rats treated with desoxycorticosterone acetate (DOCA) associated with a hypersaline diet. We measured the three substances in groups with or without parathyroid or thyroid glands, or both. Urinary phosphate excretion increased greatly during the first weeks of treatment in normal rats and in rats autografted with parathyroids and lacking thyroid, and increased slightly in the groups without parathyroids. Hydroxyproline and cAMP had the same pattern; their excretion was greatest during week 2 of treatment in all groups, but these phenomena were more intense in animals with parathyroids. These fact support the conclusion that the parathyroid glands are stimulated during the start of mineralocorticoid-saline treatment.

Animals↗
PubMed1979

Gastric antiulcer and antisecretory effects of carbenoxolone, aldosterone and desoxycorticosterone in rats.

The beneficial antiulcer actions of carbenoxolone may possibly be due to an aldosterone-like component on the gastric mucosa. This suggests that aldosterone and possibly other corticoids may have antiulcer actions. The potential gastric antisecretory and antiulcer actions of aldosterone (ALDO) and desoxycorticosterone acetate (DOCA) were studied in the rat in comparison to the reference standard carbenoxolone. Stress ulcers were induced in fasted rats by the the forced exertion technique. Gastric secretion was evaluated in the five-hour pyloric ligated Shay rat model. The renal mineralocorticoid actions of these drugs were also studied in the adrenalectomized rat. Intragastric administration of carbenoxolone and DOCA, but not ALDO, significantly inhibited gastric ulcer formation in rats. Carbenoxolone given subcutaneously (s.c.) did not inhibit ulcer formation. ALDO exhibited antiulcer actions only when multiple s.c. injections were made. The antiulcer actions of DOCA and ALDO are not mediated via an inhibitory effect on gastric secretion. At all doses tested DOCA and ALDO showed significant renal effect, while carbenoxolone exhibited this effect only at the highest tested dose. These results suggest that the beneficial antiulcerogenic action of carbenoxolone is due to a direct effect on gastric mucosa and is not related to an aldosterone-like component.

Aldosterone↗