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Biomedical subjects

P Vecsei

Publications and source records attributed to P Vecsei.

At least 109 records · Page 6Linked to original sources
PubMed1979

Dissociation in the excretion of different aldosterone metabolites and unmetabolized ('free') aldosterone in hypertension.

1. The determination of aldosterone-18-glucuronide (pH 1-labile aldosterone) was complemented by concomitant measurements of free urinary aldosterone and tetrahydroaldosterone in 307 patients, most of whom were hypertensive. In 38 cases (12.3%) the normal, aldosterone-18-glucuronide concentration was clinically misleading, but increased free aldosterone and/or tetrahydroaldosterone values suggested the presence of hyperaldosteronism, which in many of these cases was confirmed by elevated excretion of the possible major aldosterone precursor 18-hydroxycorticosterone (18-OH-B). 2. Of 224 patients with essential hypertension and normal or low plasma renin activity 18 had an elevated free aldosterone and/or tetrahydroaldosterone excretion without increased aldosterone-18-glucuronide. These cases may represent early or pre-symptomatic forms of primary hyperaldosteronism. In other cases, particularly when tetrahydroaldosterone was increased alone, abnormalities of aldosterone metabolism were suspected. 3. In two out of 15 patients with primary hyperaldosteronism, aldosterone-18-glucuronide values were frequently found to be normal, although elevations were noted in other variables. However, no relation to the morphological abnormality (adenoma versus hyperplasia) was seen.

18-Hydroxycorticosterone↗
PubMed1978

[Investigations of the plasma cortisol in psychiatric diagnostic groups (author's transl)].

In 23 endogenous depressives, 24 schizophrenics, 15 manics, 23 depressed neurotics, 23 nondepressed neurotics and 29 nonpsychiatric patients as controls, the plasma cortisol in the morning (7:30 a.m.) and the evening (7:30 p.m.) was measured with radioimmunoassay. Comparing the means of the groups, significant differences were found. In the morning the means of the nondepressed neurotics (-x = 16.6 microgram/100 ml), the endogenous depressives (-x = 14.8 microgram/100 ml), and the depressed neurotics (-x = 14.4 microgram/100 ml) are greater than that of the controls (-x = 10.0 microgram/100 ml). In the evening the means of the nondepressed neurotics (-x = 8.8 microgram/100 ml), the manics (-x = 6.4 microgram/100 ml), and the endogenous depressives (-x = 7.0 microgram/100 ml) are greater than that of the controls (-x = 3.6 microgram/100 ml); also, the mean of the nondepressed neurotics (-x = 8.8 microgram/100 ml) is greater than those of the depressped neurotics (-x = 4.9 microgram/100 ml) and the schizophrenics (-x = 4.4 microgram/100 ml). The results are compared with the literature. The interpretation of the findings is problematic: probably unspecific factors of stress and specific factors of illness--at least in depressive illness of the endogenomorphic type--are relevant.

Bipolar Disorder↗
PubMed1978

Radioimmunoassay of free urinary 18-hydroxydeoxycorticosterone (18-OH-DOC) in patients with essential hypertension.

Specific antiserum was raised in white New Zealand rabbits using 18-hydroxydeoxycorticosterone-3-oxime-BSA complex as antigen. The urinary free 18-OH-DOC was estimated after dichloromethane extraction and separation in one paper chromatographic system (propylene glycol/toluene). The mean 18-OH-DOC excretion value (+/- S.D.) in normal subjects was 0.861 +/- 0.527 microgram/24 h (n=23). ACTH produced a 25-fold increase in the excretion of free 18-OH-DOC. Dexamethasone suppressed the values to the lower range of sensitivity. 32% of patients of essential hypertension showed a moderate increase in the free urinary 18-OH-DOC values. The mean value (+/- S.D.) in the low renin hypertension group was 2.50 +/- 1.49 microgram/24 h (n=19), in the normal renin patient group 1.84 +/- 1.22 microgram/24 h (n=38). The difference between controls and the hypertensive groups was statistically significant. Among the different hypertensive groups significant differences could not be calculated.

18-Hydroxydesoxycorticosterone↗
PubMed1978

The renin-angiotensin-aldosterone system. Past, present and future.

"The present results indicate that there is a close relationship between the incretory function of the kidney, which is shown by the discharge of renin and similar materials, and the function of the adrenal cortex, especially the zona glomerulosa, which is the place of production of the sodium-retaining hormone aldosterone . Salt load inhibits the production of renin and aldosterone, while salt deprivation stimulates the production of both. The excess of sodium-retaining corticoids (DOC or aldosterone) together with sodium suppress the secretion of renin, while a deficiency of cortical hormones (adrenalectomy, morbus Addison) increase it." ... "Under these conditions the development of experimental renal hypertension could be explained as follows: the narrowing of the renal artery stimulates the secretion of renin which itself increases the formation or discharge of mineralocorticoid hormones (aldosterone or similarly acting corticoids). The resulting retention of sodium does not lead to the normal reduction of renin secretion in the ischemic kidney, so that corticoid production in the adrenal cortex is further stimulated despite no need for it."

Aldosterone↗
PubMed1978

Compounds in the urinary pH 1 extract reacting with corticosteroid and tetrahydrocorticosteroid antisera. Separation of a nonpolar substance with affinity to a tetrahydroaldosterone antiserum.

In human urinary pH 1 extracts prepared for the aldosterone-18-glucuronide estimation, several other substances are present, crossreacting not only with aldosterone antisera, but also with various corticosteroid and tetrahydrocorticosteroid antisera. Aldosterone was measured before and after chromatographic purification. Further characterization of the non-aldosterone immunoreactive material was made by immunological analysis of paper chromatogram eluats. Pregnancy, and administration of ACTH, dexamethasone, and metopirone led to a change of excretion in the antigenic equivalents. A method for the separation of the antigenic material is described. For structural elucidation the gaschromatography-mass spectrometry (GC-MS) method was applied.

Adrenal Cortex Hormones↗
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↗
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↗
PubMed1978

Simple radioimmunoassay of cortisol in diluted samples of human plasma.

We describe a simple radioimmunoassay of plasma cortisol, which can be performed in 3 h and which requires no purification, heating, or refrigeration steps. The plasma proteins are inhibited through direct competition between them and the antiserum at room temperature, at which the antiserum's affinity exceeds that of the binding proteins. Plasma, diluted with water, is incubated for 3 h at room temperature with [3H]cortisol and the antiserum. We compared results with those by the usual extraction method. The correlation between methods on evaluating normal samples with one antiserum. We compared results with those by the usual extraction method. The correlation between methods on evaluating normal samples with one antiserum was r = 0.954 (P less than 0.001), and the slope was 0.661. With three other antisera it was r = 0.922 (P less than 0.001) and slope 0.644. Plasmas with abnormal protein concentrations (i.e., from preganant women, and after corticotropin administration), tested to examine the validity of the method for routine use, and to define the role of the protein carriers, showed r = 0.859 (P less than 0.001) and slope 0.726 for the four antisera used. Additional samples, assayed with diluted standards plus stripped plasma, showed a correlation with the usual extraction method of r = 0.945 (P less than 0.001) and slope 1.026.

Cross Reactions↗