Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0338671 (Steroids)
 9,479 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The urinary excretion of 3beta,16beta-dihydroxy-5-androsten-17-one (16beta-OH-DHEA) is increased in patients with low renin essential hypertension. This steroid and its isomer 3beta,17beta-dihydroxy-5-androsten-16-one (16-oxo-A) have also been reported to have mineralocorticoid activity in adrenalectomized rats. These findings have led to the postulate that excessive secretion of 16beta-OH-DHEA may be responsible for the production of low renin essential hypertension. In this study unilaterally nephrectomized salt loaded rats injected once a week with 30 mg of 11-desoxycorticosterone acetate per/kg of body weight for 2 month periods developed hypertension. Rats given similar amounts of 16beta-OH-DHEA or 16-oxo-A and rats given no steroids did not develop hypertension. We conclude that it is unlikely that 16beta-OH-DHEA and 16-oxo-A are direct causative factors in the production of low renin essential hypertension.
Steroids 1977 Jan
PMID:Blood pressure changes following chronic administration to rats of 3beta,16beta-dihydroxy-5-androsten-17-one, 3beta,17beta-dihydroxy-5-androsten-16-one and 21-hydroxy-4-pregnene-3,20-dione-21-acetate. 13 80

A method is reported for the measurement of the urine excretion rates of tetrahydro-11-deoxycorticosterone (3 alpha,5 beta-THDOC), an important metabolite of 11-deoxycorticosterone (DOC). Quantification using gas chromatography/mass spectrometry (GC/MS) was achieved by comparing the ion fragment response for the molecular ion (m/z 507) of the analyte (as methyloxime trimethylsilyl ether derivative) to that of a fixed amount of an isomer of THDOC added to urine as internal standard. To improve the specificity of measuring THDOC in clinical samples, an additional Sephadex LH-20 chromatography step was introduced to separate 11-deoxycortisol and some progesterone metabolites. In the luteal phase of the menstrual cycle, THDOC excretion was higher than in the follicular phase; it was also higher than in women taking oral contraceptives. The correlation of THDOC with progesterone production, independent of a constant cortisol output, supports an ovarian or peripheral conversion of progesterone to DOC. The assay proved useful (1) in monitoring for the recurrence of a mineralocorticoid-secreting tumor and (2) when adrenal production of DOC was not fully suppressed in congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency. Under the latter circumstances, the renin-angiotensin system seemed to be an important regulator of DOC production.
Steroids 1992 Jan
PMID:Adrenal cortex, tumor, and peripheral production of deoxycorticosterone. 131 48

This study was undertaken to determine the secretion of aldosterone by male Long-Evans rats acclimated for six weeks to moderate cold (15 C), in comparison with rats maintained at thermo-neutral temperature (28 C). The following determinations were made: corticosteroids in plasma and adrenals, PRA, and hydromineral balance. Cold acclimation highly increased the plasma and adrenal levels of aldosterone and corticosterone. The cold stimulation of aldosterone was induced neither by the renin-angiotensin system, nor by alterations of hydromineral balance: PRA, plasma sodium and potassium concentrations, blood hematocrit, and hydromineral balance at 15 C and 28 C did not differ. Moreover this stimulation was induced neither by ACTH, nor by any other hypophyseal factors, since plasma aldosterone levels remained high in hypophysectomized rats. This study provides evidence of an aldosterone stimulation which appeared during moderate cold acclimation; the origin of this stimulation must be investigated.
Steroids 1989 Jul
PMID:Evidence for a cold-induced aldosterone stimulation in the rat. 281 57

In 2 sibs pseudohypoaldosteronism was diagnosed by measurements of high serum aldosterone and elevated plasma renin activity. During their first week of life the first born girl, phenotypically normal, went through a severe salt-losing crisis with hyponatremia and hyperkalemia. Steroids given because of suspected congenital adrenal hyperplasia had no effect. High parenteral and later oral substitution of sodium normalized the serum electrolytes. The younger brother had milder symptoms. His salt-losing crisis developing during the first week of life was treated immediately with salt substitution. Both children developed normally with high oral sodium chloride supplementation, as regulated by the parents, using daily body weight measurements. Both children frequently suffer salt-losing crises, generally preceded by simple upper respiratory tract infections, which have to be treated in the hospital by infusion with a hyperosmolar sodium chloride solution.
 ...
PMID:[Pseudohypoaldosteronism--renal salt loss syndrome. Therapy and course exemplified by 2 siblings]. 294 88

A specific radioimmunoassay (RIA) method is described for the determination of 21-deoxycorticosterone (21 DB) in human plasma. 21-Deoxycorticosterone-3-(O-carboxymethyl) oxime-bovine serum albumin conjugate was used to generate antisera in rabbits. Steroids which reacted significantly with the antisera were found to be progesterone, pregnenolone, corticosterone and 11-oxo progesterone. However, after extraction of plasma and column chromatography on Celite, all these steroids were separated from 21-deoxycorticosterone and consequently did not interfere with the radioimmunoassay. The intra- and interassays coefficients of variation were 8% and 11% respectively. Mean plasma 21-deoxycorticosterone level for healthy subjects was very low: 17.8 +/- 14.8 pmol/l (mean +/- SD) with no statistical difference between males and females. During the ACTH stimulation test, the 21-deoxycorticosterone levels of healthy subjects increased to 84.7 +/- 26.3 pmol/l (mean +/- SD) for males and 79.3 +/- 31.6 pmol/l (mean +/- SD) for females. Consequently high levels of plasma 21-deoxycorticosterone were found in treated patients suffering from congenital adrenal hyperplasia (CAH) with 21-hydroxylase deficiency, particularly in CAH salt-losers with high plasma renin activity (PRA), where the plasma level reached 40,545 pmol/l. Thus, 21-deoxycorticosterone may be a new marker for adrenal 21-hydroxylase deficiency.
 ...
PMID:The measurement of 11 beta-hydroxy-4-pregnene-3,20-dione (21-deoxycorticosterone) by radioimmunoassay in human plasma. 354 44

The relative hypertensinogenic potencies of recently synthesized 19-nor-aldosterone and its precursor 19-OH-aldosterone were assessed in comparison to that of aldosterone (Aldo) in young (6-week-old) adrenalectomized (ADX) spontaneously hypertensive rats (SHR). Infusion of 19-nor-aldosterone for 2 weeks by Alza mini-osmotic pumps caused significant, dose-dependent increases in the systolic blood pressure (BP) of young ADX SHR; dosages of 0.1 and 0.5 microgram/day raised the BP from 127 +/- 2 mmHg to 164 +/- 9 and 180 +/- 11 mmHg, respectively. During this period, control ADX SHR receiving vehicle only remained normotensive. Similar increases in BP were seen only with infusion of slightly higher dosages of Aldo (0.5 and 1.0 micrograms/day). In contrast, 19-OH-aldosterone infused at higher dosages (10 or 25 micrograms/day) caused little change in BP of ADX SHR. Full suppression of plasma renin activity (PRA) was observed with 0.1 and 0.5 microgram/day 19-nor-aldosterone, whereas Aldo caused similar decreases in PRA only at dosages of 0.5 microgram/day and higher. Interestingly, although infusions of 19-OH-aldosterone did not cause a significant change in BP, these dosages (10 and 25 micrograms/day) significantly suppressed PRA. These studies which show that 19-nor-aldosterone is equipotent to Aldo, and perhaps slightly more active in ADX SHR, indicate that 19-nor-aldosterone is a potentially important hypertensinogenic steroid.
Steroids 1985 Dec
PMID:The effects of 19-nor-aldosterone on blood pressure of adrenalectomized spontaneously hypertensive rats. 384 21

The diurnal variations of the plasma concentrations of eleven steroid hormones and of corticotropin (ACTH) were studied in ten young healthy males. The plasma steroids progesterone, pregnenolone, deoxycorticosterone, 17-OH-progesterone, 17-OH-pregnenolone, deoxycortisol, 18-OH-deoxycorticosterone, corticosterone, aldosterone, cortisol and 18-OH-corticosterone, as well as plasma ACTH, were measured at 30-min intervals in the morning and in the evening and at 2-h intervals during the rest of the day. Steroids were extracted from 1 ml plasma, fractionated by high-pressure liquid chromatography (HPLC) and finally quantified by radioimmunoassay (RIA). Plasma concentrations of ACTH were radioimmunoassayed after extraction from 2 ml plasma. More or less pronounced circadian and episodic variations were apparent for plasma levels of all steroids studied, as well as of ACTH. According to related profiles of diurnal variations of plasma concentrations, three different categories of steroids were tentatively crystallized. Category 1 includes 17-OH-pregnenolone, deoxycortisol, corticosterone, 18-OH-deoxycorticosterone, deoxycorticosterone, cortisol and 18-OH-corticosterone, exhibiting a rhythm partly synchronous with that of the pituitary secretory activity of ACTH. Category 2, including progesterone, pregnenolone and 17-OH-progesterone, exhibited a time course of plasma concentrations assuming a regulation predominantly dictated by the testicular secretory activity. Lastly, aldosterone exerted a variation of plasma concentrations which was obviously regulated by the renin-angiotensin system under the present conditions.
 ...
PMID:Diurnal and ultradian variations of plasma concentrations of eleven adrenal steroid hormones in human males. 628 2

The concentrations of aldosterone in the plasma and adrenal glands, the concentrations of sodium and potassium in the plasma and the hematocrit were estimated from birth to day 6 after birth in premature mice removed by Caesarean section on day 19 of pregnancy in comparison with newborn mice delivered spontaneously vaginally on day 20 of pregnancy. In premature mice, the plasma aldosterone concentrations increased twice: at birth after reanimation, then at 6 h after birth. The first increase at birth resulted probably from ACTH stimulation. Several factors could be involved in the peak at 6 h after birth: ACTH stimulation, the decrease in the level of sodium in the plasma and the increase in the hematocrit due to kidney immaturity of premature mice. The results suggest that the renin-angiotensin-aldosterone system is able to respond to stimulations in the first 6 h after birth in premature mice. The rise in the level of plasma aldosterone which has been found at birth in newborns delivered spontaneously vaginally on day 20 of pregnancy (control animals) did not result from variations of plasma electrolytes, plasma volume and ACTH; this rise has been induced by labor of the parturition which caused the aldosterone release from adrenal glands.
Steroids 1982 Sep
PMID:Plasma and adrenal aldosterone levels in premature mice at birth and during neonatal development. 718 5

Potassium canrenoate (K-Can) prevents hypertension in Milan hypertensive strain (MHS) but not in spontaneously hypertensive rats (SHR). Essential hypertensive patients (HT) may have differential sensitivity to diuretics, since a subgroup of HT insensitive to hydrochlorothiazide (HCTZ) but sensitive to K-Can has previously been found. The aims of this study were: 1) to seek markers of response in essential hypertensive patients selectively sensitive to K-Can: and 2) to test whether selective sensitivity to furosemide may also be demonstrated. After 2 weeks of placebo (P) 50 uncomplicated, mild to moderate HT (46 +/- 9 yrs, mean +/- SD) received K-Can (50 mg/day) for 4 weeks. After 2 more weeks of P, patients received HCTZ (25 mg) and furosemide (25 mg) for 4 weeks each in a single blind crossover design, with 2 weeks P between each treatment. Dosages were doubled after 2 weeks if diastolic blood pressure (DBP) was > 90 mmHg. Responders (R) were those HT whose DBP was < or = 90 mmHg and/or at least 10 mmHg lower than before treatment. Systolic blood pressure (SBP)/DBP was measured every 2 weeks with plasma renin activity (PRA), red blood cell Na(+)-K(+)-Cl- cotransport (COT) and Na(+)-K+ ATPase pump activity measured at the end of the first P period, and serum electrolytes at the end of each period. Four HT dropped out because of low compliance, 6 because of reversible side effects, and 1 because blood pressure was not back to pre-treatment value after the second placebo period.(ABSTRACT TRUNCATED AT 250 WORDS)
Steroids 1995 Jan
PMID:Recognition of markers of response to potassium-canrenoate in essential hypertension. 779 93

In view of the hypothetical possibility that the vascular renin-angiotensin system (RAS) might include aldosterone biosynthesis and action in the vasculature, we have undertaken a study to identify aldosterone released into the perfusion circuit from the rat mesenteric artery, and to investigate the effects of an angiotensin converting enzyme inhibition (ACEI) on aldosterone production from the vasculature. After 30 min equilibration, 240 mL of perfusate was collected and subjected to reverse-phase HPLC and subsequent mass spectrometry. Mass spectra corresponding to authentic corticosterone and aldosterone were obtained from the samples of mesenteric artery perfusate. Production of aldosterone in the mesenteric artery was not changed by adrenalectomy, although it was reduced in the arterial perfusate from rats pretreated with ACEI. By RT-PCR the expression of CYP 11B2 and mineralocorticoid receptor genes were demonstrated in both vascular endothelial and smooth muscle cells. These studies constitute indirect evidence supporting our hypothesis that locally produced aldosterone in the vascular tissue acts on vascular tone and remodeling via a paracrine or autocrine manner.
Steroids 1995 Jan
PMID:Aldosterone biosynthesis and action in vascular cells. 779 96


1 2 3 4 5 Next >>