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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
PubMed1988

24-hour serum concentration profile of cortisol in patients with Cushing's disease.

To evaluate whether or not patients with Cushing's disease can be differentiated from those with obesity by the determination of 24-hour integrated serum concentrations of cortisol we studied healthy, nonobese males (n = 5), as well as patients with marked obesity (n = 5) and with Cushing's disease (n = 7) in whom diagnosis was established biochemically and subsequently confirmed by surgery. Serum cortisol concentrations in samples collected continuously by a portable blood withdrawal pump during 24 hours (08:00-08:00h) were 6.6 +/- 1.7 micrograms/dl and 8.4 +/- 1.5 micrograms/dl in nonobese and obese individuals, respectively. Patients with Cushing's disease presented a mean cortisol concentration of 21.4 +/- 6.4 micrograms/dl (p vs normal: less than 0.005; vs obesity: less than 0.005). Collecting consecutive samples in 4-h periods the decline of serum cortisol from peak to nadir values was 73 +/- 10% and 57 +/- 23% in normal males and obese subjects, respectively, while a decline of only 22 +/- 8% was seen in patients with Cushing's disease. Three of the patients with Cushing's disease exhibited a circadian rhythm of cortisol albeit on an elevated level. These results may reflect variable stages of autonomy in pituitary ACTH-production and hence a possible criteria for differentation of hypothalamic and pituitary forms of Cushing's disease. In regard to differential diagnosis between Cushing's disease and obesity the 24-hour cortisol profile obtained by multiple sampling did not provide additional information to that obtained by a single sample pooled for 24 hours, which was diagnostic in each case.

Adrenocorticotropic Hormone↗
PubMed1988

Effect of human atrial natriuretic peptide on 1-deamino-D-Arg8-vasopressin-induced antidiuresis in man.

The interaction of exogenous synthetic human atrial natriuretic peptide (hANP), given in iv bolus doses of 100, 200, and 400 micrograms, and of various bolus-primed infusion of 1-deamino-D-Arg8-vasopressin (dDAVP), a nonpressor analog of antidiuretic hormone, were investigated in six normal men. A marked dose-dependent rise in plasma hANP concentrations occurred after the administration of hANP. The antidiuretic effect of dDAVP (P less than 0.01) was partially but not completely reversed by the concomitant administration of hANP (P less than 0.01). hANP-induced natriuresis was similar in the presence and absence of dDAVP-induced antidiuresis. While these results do not prove that hANP-dependent natriuresis and diuresis are independent phenomena, it is of clinical interest that natriuresis without diuresis can be induced by the simultaneous administration of hANP and dDAVP.

Adult↗
PubMed1987

[Detection of primary aldosteronism using the captopril test].

In order to evaluate whether changes in the plasma concentration of aldosterone (PA) following the administration of captopril, an inhibitor of angiotensin-converting enzyme, will establish the diagnosis of primary aldosteronism we have used this test in 9 healthy subjects and in 22 patients with various forms of hypertension, including 5 patients with primary aldosteronism due to idiopathic adrenal hyperplasia (n = 4) or aldosterone-producing adenoma (n = 1). The response of PA to captopril (25 mg orally) was investigated on an outpatient basis, following a rest period of 120 minutes in the supine position. In healthy subjects PA decreased from a mean basal value of 11.5 +/- 5.9 ng/dl to less than 6.4 ng/dl (4.9 +/- 1.4 ng/dl [p less than 0.01]). Similarly, captopril induced a fall in PA concentration to less than 6.4 ng/dl in patients with essential hypertension, with renal artery stenosis or with an afunctional kidney. Post-captopril concentrations of plasma aldosterone were about twice the normal level in 3 of 4 patients with idiopathic adrenal hyperplasia and about four-fold raised above normal in the patient with an aldosterone-producing adenoma. In spite of a false-negative result in one patient with idiopathic adrenal hyperplasia, the administration of captopril appears to be of use in recognizing patients with primary aldosteronism on an outpatient basis.

Adenoma↗
PubMed1987

[Human atrial natriuretic peptide: a secretory product of the heart and its significance for physiology and clinical practice].

This review deals with the physiological and clinical importance of human atrial natriuretic peptide (hANP). This peptide, which is produced by the myocardial cells of the right atrium, induces a diuretic and natriuretic response and has an inhibitory effect on aldosterone secretion. Recent elucidation of the peptide's structure represents the latest achievement in the search for an endogenous, natriuretic and hypotensive substance and has resulted in the publication of much, partly only preliminary data of its role within the homeostatic control of body sodium and water, as well as in various pathological disorders. The extensive literature is reviewed.

Aldosterone↗
PubMed1987

Prolonged administration of human atrial natriuretic peptide in healthy men: evanescent effect on diuresis in spite of simultaneous infusion of norepinephrine.

In healthy, sodium and fluid replete men (n = 6) a transient increase in diuresis is seen during the prolonged infusion of human atrial natriuretic peptide (hANP: 50 micrograms h-1 for 6 h). In order to evaluate whether this evanescent diuretic effect of hANP is due to the peptide's hypotensive action, the latter was compensated for by the concomitant infusion of norepinephrine (NE: 50 ng kg-1 min-1). The decrease in hANP-induced diuresis towards the end of the 6-h infusion was not prevented by the additional infusion of norepinephrine, which also failed to influence hANP-stimulated natriuresis. Plasma concentrations of hANP, which were continuously elevated to about double of basal concentrations during the infusion of hANP, were not affected by exogenous norepinephrine. These data demonstrate that the transient character of hANP-induced diuresis cannot be offset by counterbalancing the peptide's hypotensive effect.

Adult↗
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↗