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Biomedical subjects

H Vierhapper

Publications and source records attributed to H Vierhapper.

At least 163 records · Page 9Linked to original sources
PubMed1987

A pharmacological dose of melatonin increases PRL levels in males without altering those of GH, LH, FSH, TSH, testosterone or cortisol.

Since reports on the influence of melatonin (aMT) on the human endocrine system are scant and inconsistent, the effect of an acute, pharmacological dose of aMT on various hormone levels in healthy males was examined in 3 different experiments. Experiment I: 80 or 240 mg of crystalline aMT were administered per os to 8 volunteers. Before, during and after this treatment, serum levels of aMT, PRL, LH, FSH and testosterone were examined. Although aMT increased at least 1,500-fold over basal levels, only PRL was significantly and consistently elevated after aMT treatment, whereas serum levels of the other hormones were not altered. Experiment II: in 2 subjects, the pulsatile secretion pattern of LH was monitored for 6 h before and 6 h after aMT administration (240 mg p.o.). Neither the amplitude nor the frequency of LH pulses was influenced by the pineal hormone. Experiment III: in 14 volunteers, serum PRL, GH, TSH and cortisol concentrations were examined, once after oral administration of 240 mg aMT and once after placebo. Serum PRL levels were significantly higher after aMT than after placebo; GH showed a slight but not significant trend towards elevation after aMT, whereas other hormones were not altered. An acute pharmacological dose of aMT causes isolated elevation of serum PRL levels and may slightly increase GH. Hormones of the pituitary gonadal axis as well as TSH and cortisol are not altered by aMT.

Adult↗
PubMed1986

Effect of trilostan on steroid excretion in man: compensated inhibition of 3 beta-hydroxysteroid dehydrogenase.

Trilostan (240, 360 and 480 mg/day administered p.o. to healthy men) induced an increase (P less than 0.05) in the urinary excretion rates of DHEA, androstenediol and pregnenolone but failed to influence the excretion rates of cortisol, aldosterone, and of the four glucocorticoid metabolites, THF, allo-THF, THE and allo-THE. A rise in plasma renin concentrations was seen in the initial phase of the trial. Administration of dexamethasone in addition to trilostan suppressed plasma and urinary concentrations of cortisol and the excretion rates of all estimated steroid metabolites but did not modify the relative abundance in the excretion rates of DHEA, androstenediol and pregnenolone. These results confirm that trilostan interferes with the activity of 3 beta-hydroxysteroid dehydrogenase in man. However, under physiological conditions production of cortisol and aldosterone is kept at a constant level, most likely by compensatory stimulation of the secretion of ACTH and renin.

3-Hydroxysteroid Dehydrogenases↗
PubMed1986

Effect of prolonged administration of CRF on plasma concentrations of ACTH in patients with Addison's disease.

To investigate the possibility that the prolonged administration of corticotropin releasing factor (CRF) might suppress rather than enhance pituitary ACTH-secretion 24-hour infusions (50 micrograms/h) of ovine CRF were performed in 6 patients with adrenocortical insufficiency. CRF induced a heterogeneous behaviour of plasma ACTH concentrations in these hypercorticotropinemic patients but both a sustained increase and a suppression of ACTH was clearly absent at the end of the 24 hour infusion period. Thus, continuous administration of CRF does not appear to be a promising way to control abundance of plasma ACTH concentrations in patients with Addison's disease.

Addison Disease↗
PubMed1986

Superior efficacy of pulsatile versus continuous administration of ovine corticotropin releasing hormone in healthy man.

The effect of continuous (50 micrograms and 100 micrograms/4 hrs) versus pulsatile (6.25 micrograms every 30 minutes equivalent to a total dose of 50 micrograms during 4 hours) administration of ovine corticotropin releasing factor (oCRF) was investigated in 6 healthy, male subjects. A rise in the plasma concentrations of ACTH and of cortisol was observed during the intermittent, but not during the continuous infusion of 50 micrograms oCRF/4 hours. Comparing the rise in the plasma concentrations of ACTH and cortisol above individual basal concentrations no differences were found between the continuous infusion of 100 micrograms oCRF and the pulsatile administration of 50 micrograms oCRF. Response to pulsatile (50 micrograms/4 hrs) and continuous (100 micrograms/4 hrs) administration of oCRF, but lack of response to continuous infusion at a rate of 50 micrograms/4 hrs was also reflected by the calculated mean sum of increments of cortisol above individual basal concentrations. These results indicate a superior efficacy of intermittent versus continuous administration of oCRF in healthy man.

Adrenocorticotropic Hormone↗
PubMed1986

Unchanged pressor effect of norepinephrine in normal man following the oral administration of two angiotensin converting enzyme inhibitors, captopril and HOE 498.

The norepinephrine - (50, 100 and 200 ng/kg per min) induced rise in blood pressure (BP) was determined in six health male volunteers following angiotensin converting enzyme (ACE) inhibition by either captopril (100 mg orally) or HOE 498 (10 mg orally). In terms of absolute BP measurements both compounds induced a reduction in basal and norepinephrine stimulated BP, whereas norepinephrine induced increments of BP above individual basal levels were unchanged by either converting enzyme inhibitor. It is concluded that attenuation of the pressor response to norepinephrine does not contribute to the hypotensive action of ACE inhibitors in healthy man.

Adult↗
PubMed1986

Prolonged administration of human atrial natriuretic peptide in healthy men. Reduced aldosteronotropic effect of angiotensin II.

The effect of angiotensin II (5, 10, 20 ng/kg/min) on blood pressure and on the plasma concentrations of aldosterone was studied in six healthy men with and without the concomitant administration of synthetic human atrial natriuretic peptide given 1) as an i.v. bolus of 25 micrograms followed by a 6-hour infusion of 25 micrograms/hr or 2) as an i.v. bolus of 175 micrograms followed by a 6-hour infusion of 100 micrograms/hr. The pressor effect of angiotensin II (i.e., the rise of mean blood pressure above individual basal levels) remained unchanged during the administration of both doses of human atrial natriuretic peptide. The angiotensin II-induced rise in plasma concentrations of aldosterone in terms of absolute values) was reduced by human atrial natriuretic peptide during both trials. The rise in plasma concentrations of aldosterone above individual basal concentrations was also reduced during the administration of human atrial natriuretic peptide, although this effect was only marginal during the low dose experiment. These effects of human atrial natriuretic peptide support the contention that its therapeutic impact in hypertensive patients might be mediated in part by a reduction of high aldosterone concentrations.

Adult↗
PubMed1986

Stimulation of gonadal steroid synthesis by chronic excess of adrenocorticotropin in patients with adrenocortical insufficiency.

Analysis of 24-h urinary steroid excretion was performed by capillary gas chromatography in six patients (five men, one woman) with adrenocortical insufficiency. Ten healthy subjects (five men, five women) served as controls. A complete absence of all 21-hydroxylated steroid metabolites was seen in patients with adrenocortical insufficiency, whereas the excretion of several steroids lacking hydroxylation in the 21-position (pregnenolone, pregnenetriol, and 11-ketoandrosterone) was markedly increased. In addition, the presence of 11 beta-hydroxyandrosterone was confirmed by mass-spectrometry in the urine of three patients. This pattern of steroid excretion was unchanged in patients with adrenocortical insufficiency, both after stimulation by 1-24 adrenocorticotropin (ACTH) and after short-term (3-d) suppression with dexamethasone. We conclude that patients with adrenocortical insufficiency present a pattern of steroid excretion characterized by the absence of 21-hydroxylated metabolites. In the absence of functional adrenocortical tissue, long-term pathologically elevated concentrations of ACTH apparently stimulate early steps of steroid synthesis, most likely in the gonads. In addition, the presence of 11-hydroxylated steroid metabolites (11-ketoandrosterone, 11 beta-hydroxyandrosterone) in the urine of patients with adrenocortical insufficiency demonstrates that chronic ACTH excess in this disorder may induce some activity of 11 beta-hydroxylase, an enzyme not found in the gonads under physiological conditions.

Adrenal Cortex Diseases↗
PubMed1986

Prolonged administration of human atrial natriuretic peptide in healthy men: evanescent effects on diuresis and natriuresis.

Synthetic human atrial natriuretic peptide (hANP) was administered to six normal sodium- and fluid-replete men A) as an iv bolus dose of 25 micrograms followed by an infusion of 25 micrograms/h for 6 h; B) as an iv bolus dose of 175 micrograms; C) as an iv bolus dose of 175 micrograms followed by an infusion of 100 micrograms/h for 6 h; or D) as a continuous infusion of 100 micrograms/h for 6 h plus an iv bolus dose at 240 min. Although urinary flow rates and excretion rates of sodium and chloride increased during protocols B, C, and D, this effect either disappeared (protocol B) or waned (protocols C and D) at the end of the 6-h infusion period. A consistent decrease in blood pressure occurred only during protocols C and D. Serum concentrations of Na+, K+, and Cl- and plasma renin concentrations did not change, while plasma aldosterone concentrations declined after the administration of 175 micrograms hANP or more. These data confirm that hANP exerts a diuretic and natriuretic action in man. These effects are transient and are not maintained by prolonged continuous hANP administration.

Adult↗
PubMed1986

Effect of human atrial natriuretic peptide on angiotensin II-induced secretion of aldosterone in man.

The effect of angiotensin II (5, 10 and 20 ng/kg X min) on blood pressure and on the plasma concentrations of aldosterone was studied in 6 healthy men with and without the concomitant administration of a bolus-primed infusion (t = 6 h) of synthetic human atrial natriuretic peptide (hANP; experiment I: bolus of 25 micrograms followed by an infusion of 25 micrograms/h; experiment II: bolus of 175 micrograms followed by an infusion of 100 micrograms/h). The pressor effect of angiotensin II (i.e.: the rise of mean blood pressure above individual basal levels) remained unchanged during the administration of both doses of hANP. The angiotensin II-induced rise in plasma concentrations of aldosterone was reduced by hANP during both trials. Hence, the therapeutical impact in hypertensive patients might, in part, be mediated via reduction of high aldosterone concentrations.

Adult↗
PubMed1985

Effect of indomethacin on hepatic glucose production in vitro: the impact of hepatic glycogen content.

The effect of indomethacin (IND) on glucagon-induced hepatic glucose production (HGP) was studied in the isolated perfused livers of rats. Addition of IND (0.2 mM) to the perfusion medium had no effect on glucagon-stimulated HGP when compared to control experiments without added IND (1.02 +/- 0.17 vs. 1.00 +/- 0.26 mmol per (120 min X 100 g b.w.), respectively; NS). Intravenous pretreatment with both, IND (10 mg/kg b.w.), or vehicle resulted in a reduction in glucagon-induced HGP due to a decrease in hepatic glycogen content. A complete depletion of the hepatic glycogen pool and thus a lack in glucagon-stimulated HGP was observed when IND was given intraperitoneally. These results indicate that the changes in HGP observed after pretreatment with IND may largely if not completely be due to a non-specific depletion in hepatic glycogen content and that IND does not exert a direct influence on HGP.

Animals↗
PubMed1985

[Corticotropin releasing factor as an aid in the diagnosis of Cushing syndrome].

6 patients with Cushing's syndrome were investigated with regard to the effect of synthetic ovine corticotropin-releasing factor (o-CRF), administered as an intravenous bolus of 100 micrograms, on peripheral plasma concentrations of ACTH and cortisol. The purpose of this study was to evaluate the usefulness of this "CRF test" in the differential diagnosis of Cushing's syndrome as compared with conventional diagnostic procedures. 100 micrograms CRF caused a rise in plasma ACTH and cortisol in patients with bilateral adrenal hyperplasia (n = 3). However, in patients with cortisol-producing adrenal adenoma (n = 2) and ectopic ACTH overproduction (n = 1), no increase in plasma cortisol and ACTH was induced by exogenous CRF. We conclude from these findings that the CRF test will prove a valuable diagnostic tool to differentiate pituitary from extrapituitary forms of endogenous hypercortisolism in patients with Cushing's syndrome.

Adolescent↗
PubMed1985

Acetyl-salicylic acid impairs insulin-mediated glucose utilization and reduces insulin clearance in healthy and non-insulin-dependent diabetic man.

The effect of acetyl-salicylic acid (ASA, 3 g per day for 3 days) on glucose utilization and insulin secretion was studied in healthy volunteers and Type 2 diabetic patients using the hyperglycaemic and euglycaemic insulin clamp technique. When in healthy subjects arterial plasma glucose was acutely raised and maintained at +7 mmol/l above fasting level, the plasma insulin response was enhanced by ASA (70 +/- 7 vs. 52 +/- 7 mU/l), whereas the plasma C-peptide response was identical. Despite higher insulin concentrations, glucose utilization was not significantly altered (control, 61 +/- 7; ASA, 65 +/- 6 mumol X kg-1 X min-1) indicating impairment of tissue sensitivity to insulin by ASA. Inhibition of prostaglandin synthesis was not likely to be involved in the effect of ASA, since insulin response and glucose utilization were unchanged following treatment with indomethacin. In the euglycaemic insulin (1 mU X kg-1 X min-1) clamp studies, glucose utilization was unaltered by ASA despite higher insulin concentrations achieved during constant insulin infusion (103 +/- 4 vs. 89 +/- 4 mU/l). In Type 2 diabetic patients, fasting hyperglycaemia (10.6 +/- 1.1 mmol/l) and hepatic glucose production (15 +/- 2 mumol X kg-1 X min-1) fell upon ASA treatment (8.6 +/- 0.7 mmol/l; 13 +/- 1 mumol X kg-1 X min-1). During the hyperglycaemic clamp study, the plasma response of insulin, but not of C-peptide, was enhanced by ASA, whereas tissue sensitivity to insulin was reduced by 30 percent.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1985

Capillary gas chromatography as a tool for characterization of urinary steroid excretion in patients with congenital adrenal hyperplasia.

Urinary steroid excretion was studied by capillary gas chromatography in 23 patients with congenital adrenal hyperplasia. In 5 patients the estimated excretion rates of pregnanetriol were in or below the normal range and 7 patients presented supranormal excretion rates of tetrahydro-cortisone and/or other glucocorticoid metabolites. Deficiency of 21-hydroxylase was nevertheless demonstrated in each patient by an increased ratio of excreted precursors vs products of 21-hydroxylase, e.g. of pregnanetriol/tetrahydro-cortisone. Due to this relative deficiency of glucocorticoids the patients' steroid excretion was further characterized by a predominance of 5 alpha-hydrogenated C19O3 metabolites (11-keto-androsterone, 11-hydroxy-androsterone) over their 5 beta-hydrogenated homologues (11-keto-etiocholanolone, 11-hydroxy-etiocholanolone). An apparent preponderance in the excretion of pregnenetriol over that of pregnanetriol was found in 4 patients, but the presence of pregnenetriol was not confirmed by mass spectrometry following prepurification of the urine samples by thin-layer chromatography indicating interference of an unidentified steroid metabolite with the initial gas chromatographic analysis. The simultaneous determination of steroids serving as precursors or products of 21-hydroxylase by capillary gas chromatography helps to establish the diagnosis of 21-hydroxylase deficiency and to characterize the pattern of steroid excretion in this syndrome even in patients where the estimation of single urinary steroids may lead to erroneous conclusions.

Adolescent↗
PubMed1985

Generation of prostaglandin E2-like radioimmunoreactive material in human plasma during storage at -20 C but not at -80 C.

Concentrations of prostaglandin E2 (PGE2) as determined by radioimmunoassay following silicic-acid column chromatography in extracted samples (n = 5) of human plasma (Na2EDTA: 18 mg/5 ml blood; indomethacin: 1mg/5 ml blood) were less than 1.0 pg/ml when the samples were extracted immediately after blood withdrawal. Virtually identical concentrations of PGE2 were determined in samples stored at -80 degrees C for up to 6 months. However, when the same analytical procedures were used after prolonged storage of the plasma samples at -20 degrees C an apparent rise in the estimated plasma concentrations of PGE2 up to 5.1 +/- 1.9 pg/ml (3 months) and to 25.2 +/- 7.8 pg/ml, (6 months) was observed. Repeated freezing and rethawing of 4 plasma samples within 48 hours after blood withdrawal did not influence concentrations of PGE2 thus excluding acute destruction of residual platelets as the cause of the observed time-dependent rise in radioimmunologically determined 'PGE2'. Two plasma samples stored at -20 degrees C for 26 months were subjected to HPLC subsequent to silicic acid column chromatography. Radioimmunoassay of PGE2 performed for each eluted fraction resulted in 3 distinct peaks of "PGE2"-like activity, suggesting heterogeneity of cross-reacting compounds generated during prolonged storage at -20 degrees C. In conclusion, to determine concentrations of PGE2 in human plasma by means of radioimmunoassay the samples should either be extracted immediately after blood withdrawal or be kept at -80 degrees C.

Adult↗
PubMed1985

Contribution by the glycogen pool and adenosine 3',5'-monophosphate release to the evanescent effect of glucagon on hepatic glucose production in vitro.

To elucidate in vitro the transience of glucagon-induced hepatic glucose release, the effects of glucagon on hepatic glucose production and cAMP release were evaluated in the isolated rat liver preparation perfused by a nonrecirculating system. Glucagon was added to the infusate in stepwise increasing concentrations at 0, 60, and 100 min to give final concentrations of 2.5 X 10(-11), 10(-9), and 5 X 10(-8) M, respectively. Glucagon at 2.5 X 10(-11) M caused cAMP release [basal (mean +/- SD), 11.2 +/- 3.0 pmol/(min X 100 g BW)] to rise rapidly and plateau at 23.3 +/- 7.0 pmol/(min X 100 g BW), whereas hepatic glucose production [basal, 3.7 +/- 1.6 mumol/(min X 100 g BW)] increased only transiently to a maximum of 15.3 +/- 3.1 mumol/(min X 100 g BW) and fell thereafter. The enhanced cAMP release during the consecutive glucagon infusion was accompanied by a transient rise in hepatic glucose production during the second, but not during a third, glucagon infusion. When 3-isobutyl-1-methylxanthine, a potent phosphodiesterase inhibitor, was added to the perfusion medium (0.5 mM), the cAMP response to 2.5 X 10(-11) M glucagon was enhanced [247 +/- 124 pmol/(min X 100 g BW)] as was hepatic glucose production (+ 21%; P less than 0.05). Further augmentation of the glucagon concentration was followed by an increase in hepatic cAMP, but not glucose, release. When glucagon infusion (2.5 X 10(-11) M) was repeated with a glucagon-free period of 30 min in between, no stimulation of cAMP and consecutive glucose release was found during the second period. However, when the second glucagon dose was increased to 10(-9) M, glucose and cAMP release were again stimulated to the same extent as in experiments with no glucagon-free period in between. We conclude that the size of the glycogen pool and the cAMP concentration directly modulate hepatic glucose production and are responsible for evanescent glucagon action. This mechanism can be described by computer simulation.

1-Methyl-3-isobutylxanthine↗