THE EFFECT OF ADRENAL STIMULATION WITH ADRENOCORTICOTROPHIC HORMONE ON THE EXCRETION OF DEHYPROISOANDROSTERONE IN MAN1,2,3,4,5,6

Landau, Richard L.; Knowlton, Kathryn; Lugibihl, Kathleen; Kenyon, Allan T.

doi:10.1210/endo-48-5-489

Cited by 16 publications

(7 citation statements)

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“…Despite the marked rise, it should be noted that the amount of this ,8-ketosteroid did not parallel the response to ACTH as determined by either the 11-oxygenated or 1 1-desoxy a-ketosteroids. Thus, while both dehydroisoandrosterone and "dehydroisoandrosterone like substances" increase during adrenal stimulation with ACTH (12)(13)(14), it can be suggested from the disparity in the quantitative response of a and ,8 ketosteroids that different precursor-product mechanisms may be involved in the elaboration and excretion of these various compounds.…”

Section: Methodsmentioning

confidence: 99%

STUDIES IN STEROID METABOLISM. XXVIII. THE Α-Ketosteroid EXCRETION PATTERN IN NORMAL FEMALES AND THE RESPONSE TO ACTH 1

Kappas¹,

Gallagher²

1955

J. Clin. Invest.

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An examination of the urinary a-ketosteroids has been made in normal women in order to provide information about this important group of hormone metabolites. These data establish limits of values for the major components of this group of steroids and thus provide not only a suitable comparison for studies in abnormal or altered hormonal physiology, but offer information about possible sex differences in the composition of these hormonal metabolites as well. The qualitative and quantitative a-ketosteroid excretion pattern of a series of normal males has been reported earlier from this laboratory (1).Two of the pre-menopausal women were studied at successive intervals throughout the menstrual cycle. The results provide evidence that the precursors of the major urinary neutral ketosteroids in normal women are secreted independently of this pituitary-ovarian rhythm. In addition, two other normal young women were studied during control periods as well as during successive periods while under vigorous stimulation with adrenocorticotrophic hormone (ACTH). The results provide information on the character of this adrenal response in women, and are thus helpful in the interpretation of abnormal hormonal situations, an example of which is described in a recent study (2).The development of methods for more satisfactory hydrolysis of urinary steroid conjugates, improvement in the techniques of separation, particularly partition column and paper chromatography

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Section: Methodsmentioning

confidence: 99%

STUDIES IN STEROID METABOLISM. XXVIII. THE Α-Ketosteroid EXCRETION PATTERN IN NORMAL FEMALES AND THE RESPONSE TO ACTH 1

Kappas¹,

Gallagher²

1955

J. Clin. Invest.

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“…

Progesterone has been reported to be natriuretic ( 1 4 ) and catabolic (4-6) in man. Both in vivo (3,4) and in vitro (9) studies suggest that the natriuretic effect is through the blocking of aldosterone action. Progesterone was also shown to elevate peripheral plasma renin activity (PPRA) in the dog (8).

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confidence: 99%

“…Progesterone has been reported to be natriuretic ( 1 4 ) and catabolic (4)(5)(6) in man. Kagawa et al (7) demonstrated natriuresis in the rat.…”

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confidence: 99%

Metabolic Effects of Progesterone in the Dog

O'Connell

Boonshaft

Hayes

et al. 1969

Experimental Biology and Medicine

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Progesterone has been reported to be natriuretic ( 1 4 ) and catabolic (4-6) in man. Kagawa et al. (7) demonstrated natriuresis in the rat. Progesterone was also shown to elevate peripheral plasma renin activity (PPRA) in the dog (8). Both in vivo (3,4) and in vitro (9) studies suggest that the natriuretic effect is through the blocking of aldosterone action. The purpose of the present investigation was to study the metabolic effects of progesterone in the dog and attempt to correlate them with changes in PPRA.Materials and Methods. Four female mongrel dogs, weighing 16-25 kg, were maintained in metabolic cages; and complete 24-hr urine collections were obtained by daily bladder catheterizations. The dogs were initially placed on a sodium diet containing approximately 3 5-40 meq (normal sodium diet) for 30 days. On this diet PPRA was assayed on alternate days and daily urinary sodium and urea excretion were measured. After initial stabilization, a synthetic proges-terone4 (200 mg, im/day) was administered for 6 days. The dogs were then allowed to stabilize for another 6 days and an aldosterone antagonist (spironolactone, 300 mg/ day, po) was administered in the diet for 5 days. The dogs were then placed on a sodium diet containing 3-6 meq/day (low sodium diet) and were allowed to stabilize for one week. The same studies utilizing prowith certification of chemical analysis. 40 VI CT I N 30 z CONTROL RECOVERY L --63 S P I R O N O L A C T O N E 0 , -; ; 20 v -x W 5 3 10 n 0 VI 0 N O R M A L LOW S O D I U M D I E T S O D I U M D I E T FIG. 1. Effects of progesterone and spironolactone on sodium excretion.gesterone and spironolactone were then repeated on this diet.The bloods for PPRA were drawn into heparinized tubes and immediately centrifuged in the cold, and the plasma was separated and frozen. The PPRA was measured by a modification of the method of Helmer ( 10) as described by Boonshaft et al. (1 1).Renin activities are expressed in terms of nanograms of angiotensin I1 generated per milliliter of plasma per hour of incubation. Urinary sodium was determined with an IL flame photometer using an internal lithium standard. Urinary urea was measured by the urease method ( 12 ) .Results. On the normal sodium diet, the control sodium excretion was 37.4 t 1.3 meq/24 hr (mean t SEM) and the control urea excretion was 5.71 t 0.38 gJ24 hr. After progesterone administration, the sodium excretion was 32.2 -+ 1.9 meq/24 hr ( p > .05) and the urea excretion was 5.65 t_ 0.29 g/24 hr (Table I) which also was not significant ( p > .05). After spironolactone administration, the urinary sodium excretion was 37.2 t 2.3 meq/24 hr (Fig.

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“…Since the excretion of large amounts of dehydroisoandrosterone in the urine has always been found in association with adrenal hyperactivity, e.g., following stimulation of the adrenals with ACTH (5,12), the precursors of this metabolite must be sought among the steroids elaborated by the adrenal cortex. The exact chemical nature of this precursor, it seems to us, can be surmised from an examination of the chemical nature of some of the urinary steroids, together with a consideration of the mechanism of biogenesis of the adrenal hormones.…”

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confidence: 99%

Metabolic Precursors of Urinary Dehydroisoandrosterone

Lieberman

Teich

1953

The Journal of Clinical Endocrinology & Metabolism

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E VER since dehydroisoandrosterone was first isolated from human urine in 1934 (1) the riddle of its precursor has plagued the biochemist and the clinician. Since it has recently been shown that dehydroisoandrosterone is excreted in normal urine in much larger amounts than hitherto recognized, and therefore that this substance is an important index of normal as well as abnormal adrenal cortical activity, the question of its precursor has assumed added importance. Especially is this true since the estimation of urinary dehydroisoandrosterone is probably as significant for evaluating adrenal cortical function as the determination of urinary corticoids.It is unnecessary to dwell upon the reasons why earlier workers reported low excretion values (of the order of 0.2 mg. /day) (2) in the urine of normal men and women. It is well recognized now that vigorous acid hydrolysis alters a sensible fraction of the dehydroisoandrosterone sulfate present in any urine, resulting in an underestimation of the actual concentrations. Nevertheless a recent paper by Landau et al. (3) reported that normal men and women excreted 1.0-12.4 mg./twenty-four hours, or 10-60 per cent of the total ketosteroids, even when using a l^drolytic procedure consisting of boiling with acid for fifteen minutes. Dingemanse et al. (4) estimated from a chromatographic analysis of the urinary 17-ketosteroids that normal women excreted on the average 1.4 mg. of dehydroisoandrosterone daily (about 30 per cent of the total ketosteroids) and normal men, 2.6 mg. of the steroid daily (about 50 per cent of the total). Using a mild method of acid hydrolysis, Ronzoni (5) isolated the ketonic, digitoninprecipitable fraction and measured its deh}^droisoandrosterone content by the Allen test (6). By this procedure she estimated the normal excretion of this adrenal metabolite to be 2.2-5.0 mg./twenty-four hours or 15-26 per cent of the total 17-ketosteroids.Although attempts have been made to examine certain steroids as possible precursors of urinary dehydroisoandrosterone, the nature of these precursors remains obscure. In spite of the superficial similarity in chemical structure between the hormone, testosterone, and the metabolite, dehydroisoandrosterone, it was recognized early that the hormone was not the 1140

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THE EFFECT OF ADRENAL STIMULATION WITH ADRENOCORTICOTROPHIC HORMONE ON THE EXCRETION OF DEHYPROISOANDROSTERONE IN MAN¹^,²^,³^,⁴^,⁵^,⁶

Cited by 16 publications

References 0 publications

STUDIES IN STEROID METABOLISM. XXVIII. THE Α-Ketosteroid EXCRETION PATTERN IN NORMAL FEMALES AND THE RESPONSE TO ACTH 1

STUDIES IN STEROID METABOLISM. XXVIII. THE Α-Ketosteroid EXCRETION PATTERN IN NORMAL FEMALES AND THE RESPONSE TO ACTH 1

Metabolic Effects of Progesterone in the Dog

Metabolic Precursors of Urinary Dehydroisoandrosterone

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