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Biomedical subjects

W Rauh

Publications and source records attributed to W Rauh.

At least 37 records · Page 2Linked to original sources
PubMed1980

New studies of the 11 beta-hydroxylase and 18-hydroxylase enzymes in the hypertensive form of congenital adrenal hyperplasia.

Studies in four children with congenital adrenal hyperplasia due to 11 beta-hydroxylase deficiency provide evidence for two separate 11 beta-hydroxylating systems in the adrenal zona fasciculata and zona glomerulosa. In addition, these studies support the proposal that the adrenal 11 beta- and 18-hydroxylating activities are related and may involve the same enzyme protein and catalytic site. In the untreated or poorly treated state, despite elevation of deoxycorticosterone (DOC) and tetrahydrodeoxycorticosterone, urinary free 18-hydroxy-DOC was in the low normal range and did not increase normally with ACTH. PRA and urinary free 18-hydroxycorticosterone (18-OHB), tetrahydroaldosterone (TH Aldo), and pH 1 aldosterone were suppressed in the untreated and ACTH periods. Glucocorticoid administration suppressed plasma ACTH, and urinary tetrahydro-DOC and free DOC excretion decreased to the normal range. Concomitantly, there was a rise in PRA accompanied by parallel increase in urinary 18-OHB, urinary TH Aldo, and pH 1 aldosterone. While on dexamethasone, a low sodium diet (10 meq/day) resulted in prompt sodium retention, with a further rise in PRA and urinary 18-OHB, TH Aldo, and pH 1 aldosterone. These studies indicate the presence of both an 11 beta- and an 18-hydroxylase deficiency in the zona fasciculata and normal 11 beta- and 18-hydroxylase function in the zona glomerulosa, suggesting that these two enzymatic functions are related and that separate enzyme systems are present in the two zones.

Adolescent↗
PubMed1979

6 beta-Hydroxycortisol excretion in hypercortisolemic states.

Urinary 6beta-hydroxycortisol (6betaOHF) excretion was measured and compared with free cortisol and 17-hydroxycorticosteroid (17OH) excretion in normal children, patients with Cushing's syndrome or disease (CSD), and patients during cortisol therapy. Normal 6betaOHF excretion in children was 0.23 +/- 0.03 mg/m2/24 h (mean +/- SE). No sex difference was found. ACTH infusion (40 U/day for 5 days) and high dose cortisol altered the 6 betaOHF:17OH ratio so that it was indistinguishable from the ratio seen in CSD. The fact that both Cushing's disease and high dose cortisol therapy caused the same change in the 6 betaOHF:17OH ratio suggests that cortisol and not ACTH induced 6beta-hydroxylase in hypercortisolemic subjects. Since the 6betaOHF:17OH ratio in CSD patients was always well above the normal range, measurement of 6betaOHF excretion was a better and more rapid test for chronic hypercortisolemia than urinary 17OH or free cortisol. Thus, measurement of urinary 6betaOHF is suggested as a good diagnostic test for hypercortisolemic states.

17-Hydroxycorticosteroids↗
PubMed1979

Adrenocortical function, electrolyte metabolism, and blood pressure during prolonged adrenocorticotropin infusion in juvenile hypertension.

The effect of a continuous 5-day ACTH infusion (40 U/24 h) on adrenocorticoid function, electrolyte metabolism, and blood pressure was investigated in eight normotensive children and eight patients with hypertension of unknown origin. There was a continuous rise of plasma cortisol and deoxycorticosterone in all patients. Plasma aldosterone rose transiently in the normotensive and the hypertensive group. A transient kaliuresis and a continuous fall in serum K+ were observed in all patients. ACTH induced sodium retention and weight gain. The observed increase in systolic blood pressure correlated significantly with the cumulative sodium retention in the normotensive and the hypertensive groups. No correlation between sodium retention and diastolic pressure was found. ACTH on a low salt diet (10 meq/24 h) produced a blood pressure rise which was smaller than that on regular salt. The blood pressure rise did not correlate with any of the hormones measured. This study provides evidence for an unidentified ACTH-stimulable adrenal factor capable of raising blood pressure in normotensive children and patients with juvenile hypertension. The ACTH-induced blood pressure rise is only partly salt dependent and the mechanism of the rise remains unclear.

Adolescent↗
PubMed1979

A syndrome of apparent mineralocorticoid excess associated with defects in the peripheral metabolism of cortisol.

A syndrome is described whose features, suggestive of primary mineralcorticoid excess, included hypertension, hypokalemia, low PRA, and responsiveness to spironolactone. Aldosterone levels were subnormal but as yet there has been no evidence of overproduction of other mineralocorticoids by chemical analysis or by bioassay of plasma and urinary extracts. The steroidal abnormalities that were observed involved peripheral matabolism rather than secretion. One patient exhibited a transient delay in reduction of the 3-keto group in the A ring, and both patients exhibited a decrease in the metabolism of cortisol to biologically inactive cortisone. This was shown by the marked decrease in the excretion of urinary metabolites bearing an 11-keto group and a decrease in the oxidation of 11 alpha-[3H]cortisol to tritiated water. The defect appeared not to be a deficiency of the 11 beta-oxidoreductase system itself, since the reverse reaction of conversion of cortisone to cortisol proceeded normally, but, rater, an alteration in the equilibrium position of 11 beta-oxidoreduction in favor of the reduced form. This was also expressed by a prolongation of the half-time of disappearance of cortisol. The decrease in the MCR permitted the maintenance of normal cortisol plasma levels and normal glucocorticoid function at a diminished rate of secretion. The decreased rate of conversion of cortisol to cortisone serves as a biochemical marker of this hypertensive syndrome.

17-Hydroxycorticosteroids↗
PubMed1978

Mineralocorticoids, salt balance and blood pressure after prolonged ACTH administration in juvenile hypertension.

The effect of a 5 day ACTH test (40 U/24 h) on plasma aldosterone (aldo), deoxycorticosterone (DOC), plasma renin activity (PRA) and urinary excretion of aldosterone-pH1-conjugate (pH-1-aldo) and tetrahydro-DOC (TH-DOC) was investigated in 8 normotensive children (group I), 8 patients with hypertension of unknown origin (group II), and 4 hypertensive children with dexamethasone suppressible hyperaldosteronism (DSH) (group III). Changes in blood pressure and sodium balance were studied in all groups. Under baseline conditions there was no hormonal difference between group I and II. In contrast, the children in group III had a suppressed PRA and a 1.5--2 fold elevation of aldo and DOC. Plasma DOC and urinary THDOC increased continuously 10--50 fold in all groups during the ACTH test. Aldo rose transiently 2--4 fold on the first day of ACTH and fell subsequently below baseline levels in group I and II. The children with DSH (group III), however, showed an unusual, sustained aldo stimulation with ACTH. PRA decreased significantly after ACTH in group I and II. Sodium retention aTH administration. The highest blood pressure rise was observed in group III (from 124/72 to 139/90 mm Hg). The blood pressure response to ACTH was partly sodium dependent. Although aldo and DOC and sodium retention may contribute to the ACTH induced blood pressure elevation, other factors must play a role.

Adolescent↗
PubMed1978

[Adrenal function after long term treatment with beclomethasone dipropionate in childhood asthma (author's transl)].

Evaluating plasma levels of cortisol and corticosterone after ACTH-stimulation, and the urinary metabolites tetrahydrocortisone and tetrahydrocortisol in asthmatic children it could be demonstrated, that in most cases there was no suppression of adrenal function following treatment over 6 to 18 months with a daily dose of 200 to 300 microgram beclomethasone dipropionate. Since in a few patients suppression was found, an ACTH stimulation after a six months treatment is recommended.

Adolescent↗
PubMed1975

The renin-angiotensin system in acute renal failure of rats.

1. Acute renal failure was produced in rats by intramuscular injection of glycerol. Subsequently, changes in the concentrations of renin and of angiotensin II in plasma and the renin content of the kidneys were followed. 2. at 4 and 8 h after glycerol administration, plasma renin and angiotensin II had increased two to three-fold; they remained elevated for 48 h and then returned towards normal. At 7 days, the values were still slightly raised. 3. At 4 and 8 h after glycerol injection, kidney renin had decreased but it had increased after 24 and 48 h. 4. Passive immunization with angiotensin II antibodies, given at the time of glycerol injection and 2 and 4 h afterwards, prevented the development of acute renal failure. When angiotensin II antiserum was administered later (8, 10 and 12 h after glycerol) it had no effect. 5. Stimulation of the renin-angiotensin system may be involved in the pathogenesis of the early phase of acute renal failure.

Acute Kidney Injury↗