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Biomedical subjects

E Jungmann

Publications and source records attributed to E Jungmann.

At least 109 records · Page 6Linked to original sources
PubMed1986

Evidence for increased endogenous dopaminergic inhibition of aldosterone secretion in prolactinoma.

Aldosterone responsiveness to consecutive i.v. injections of metoclopramide 1 mg, 2.5 mg and 10 mg was studied in 8 patients with prolactinoma and normally preserved adrenal function and in 14 healthy volunteers. In the patients, aldosterone response to metoclopramide 1 mg was blunted. After metoclopramide 10 mg, aldosterone rose to the same levels in patients and volunteers. In the patients, however, percentage rise of aldosterone was enhanced, since the appropriate base line concentration of aldosterone was decreased. Thus, there is evidence for increased endogenous dopaminergic inhibition of aldosterone secretion in prolactinoma.

Adult↗
PubMed1986

Human atrial natriuretic peptide (hANP) has no effect upon dopaminergic pathways: preliminary evidence in nude mice bearing heterotransplanted human CONN's adenoma tissue.

To examine whether human atrial natriuretic peptide (hANP) has an agonistic effect on dopaminergic pathways, we studied the natriuretic action and the suppressive effect of hANP on aldosterone secretion before and during treatment with haloperidol or pergolide in nude mice harbouring heterotransplanted human CONN's adenoma tissue. Nude mice with heterotransplanted tumour material without hormonal activity served as controls. The natriuretic efficacy of hANP remained unchanged by haloperidol or pergolide both in controls and in nude mice with heterotransplanted CONN's adenoma tissue. On the other hand, hANP had no effect upon the haloperidol-induced increase in aldosterone excretion in the control animals. Thus, preliminary evidence emerges that hANP has no effect on dopaminergic pathways and that the aldosterone inhibiting action of hANP is only of minor physiological significance.

Adenoma↗
PubMed1986

[Effect of captopril in chronic aortic insufficiency].

In 16 patients with chronic aortic regurgitation, we studied the acute hormonal and hemodynamic effects of 12.5 to 25 mg captopril; in 12 patients the changes after a 4 to 8 week treatment period (mean 6.3 +/- 2 weeks; doses: 3 times 12.5 to 3 times 25 mg/day) were investigated. The following baseline variables were evaluated: the radionuclide left ventricular ejection fraction (EF) at rest and during exercise, left ventricular end-diastolic volume (EDV), regurgitant blood volume (RBV); and plasma renin activity (PRA). Repeated determinations of EF, EDV and RPA were carried out 90 minutes after application of the drug. In patients with chronic therapy, EF at rest and during exercise, EDV, RBV and PRA were reinvestigated at the end of the study. Acute administration of captopril was followed by an increase of EF (from 49 +/- 12 to 55 +/- 12%, p less than 0.001) and a slight decrease of EDV (from 389 +/- 160 to 376 +/- 146 ml, p less than 0.05). PRA significantly increased (from 1.6 to 3.1 ng/ml/h, p less than 0.05). Chronic therapy resulted in a moderate decrease of systolic and diastolic blood pressure (from 156/70 +/- 31/15 to 140/63 +/- 23/15 mm Hg, p less than 0.01). However, no significant changes were observed in EF at rest and during exercise (51 +/- 9 vs. 53 +/- 10% and 45 +/- 14 vs. 47 +/- 14%), EDV (433 +/- 179 vs. 422 +/- 179 ml) and RBV (136 +/- 81 vs. 129 +/- 77 ml). PRA was significantly increased (6.3 ng/ml/h, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Aortic Valve Insufficiency↗
PubMed1985

Aldosterone and prolactin responsiveness after prolonged treatment of congestive heart failure with captopril.

After long-term captopril treatment, an inappropriate increase in aldosterone levels has been observed in hypertensive patients. It is not known, whether a similar change would occur in patients with severe congestive heart failure, and whether it is due to a decrease in endogenous dopaminergic inhibition of aldosterone secretion or to aldosterone stimulation by ACTH or an ACTH-related peptide. Therefore, the aldosterone and prolactin responses to metoclopramide have been studied in 10 patients with severe congestive heart failure (NYHA Class III or IV) after 6 months of captopril treatment, before and 11 h after pretreatment with dexamethasone. 7 placebo-treated patients served as double-blind controls. In captopril-treated patients, the supine aldosterone levels exceeded the normal range and were as high as in placebo-treated patients. The responsiveness of aldosterone and prolactin to metoclopramide was not influenced by captopril. Only in the placebo group were the aldosterone levels decreased by dexamethasone. Captopril increased plasma renin activity and serum potassium, and decreased supine epinephrine and norepinephrine and serum sodium. Thus, previous reports of inappropriately high aldosterone levels after long-term captopril treatment were confirmed in patients with severe congestive heart failure. It is concluded that increased aldosterone is due neither to a decrease in endogenous dopaminergic inhibition nor to dexamethasone-suppressible stimulation of aldosterone secretion.

Adult↗
PubMed1984

The effect of pizotifen, a serotonin antagonist, and of pirenzepine, a muscarinic antagonist, on hormonal responses to metoclopramide in healthy subjects.

To examine whether and how muscarinic or serotoninergic properties might contribute to the hormone stimulating action of the dopamine antagonist metoclopramide, the effect of oral single-dose pretreatment with pirenzepine (Gastrozepin) 50 mg, a muscarinic antagonist, pizotifen (Sandomigran) 1 mg, a serotonin antagonist, or placebo on the responses of prolactin, aldosterone, plasma renin activity (PRA), cortisol (hydrocortisone) and human growth hormone (HGH) to the i.v. injection of metoclopramide 10 mg was studied in 6 young healthy volunteers. For comparison, a mere placebo study was added. Whereas aldosterone response to metoclopramide and PRA remained unchanged, prolactin response was decreased by pizotifen from 43 +/- 6.5 to 24 +/- 9 ng/ml, p less than 0.05. Pizotifen decreased base-line cortisol from 10.5 +/- 0.5 to 6.6 +/- 0.6 microgram/dl and prevented the increase in cortisol after metoclopramide in responsive subjects. Both pizotifen and pirenzepine decreased HGH responsiveness to metoclopramide. It is concluded that cortisol and, partly, prolactin stimulation by metoclopramide are due to its serotoninergic properties and that HGH responsiveness to metoclopramide becomes explainable by both the serotoninergic and muscarinic potencies of the drug.

Adult↗
PubMed1983

The effect of metoclopramide and haloperidol on plasma renin activity and aldosterone levels in rats.

To gain further information on dopaminergic inhibition of renin release and aldosterone secretion, we studied the effect of 0.1, 1.0, or 5.0 mg metoclopramide or haloperidol/kg body weight i.p. on plasma renin activity (PRA) and aldosterone concentration in serum, and of furosemide pretreatment or dietary sodium restriction (14 days) on PRA and aldosterone responses to 1.0 and 5.0 mg haloperidol/kg b.wt. i.p. in groups of eight male Sprague-Dawley rats. Aldosterone levels in serum were increased very similarly by 0.1 and 1.0 mg metoclopramide and haloperidol/kg. Whereas PRA and aldosterone were unaffected by 5.0 mg metoclopramide/kg, both were maximally stimulated by 5.0 mg haloperidol/kg. Furosemide pretreatment increased PRA and aldosterone concentration and blunted the aldosterone response to haloperidol. PRA response to 5.0 mg haloperidol/kg was not changed. After sodium restriction, aldosterone concentration as inappropriately high and did not respond to 1.0 mg haloperidol/kg. However, PRA and aldosterone response to 5.0 mg haloperidol/kg was magnified. Our study confirms both dopaminergic inhibition of PRA and stimulation of aldosterone secretion by dopamine antagonists in rats. A feedback regulatory mechanism becomes conceivable which comprises aldosterone secretion, sodium turnover, volume homeostasis, and dopaminergic activity.

Aldosterone↗
PubMed1983

The inhibiting effect of trilostane on testosterone synthesis. Hormonal and morphologic alterations induced by subchronic trilostane treatment in rats and healthy volunteers.

(2 alpha, 4 alpha, 5 alpha, 17 beta)-4, 5-[Epoxy-17-hydroxy-3-oxo-androstane-2-carbonitrile (Trilostane, Win 24450) is a new, orally active, competitive inhibitor of 3 beta-hydroxysteroid dehydrogenase currently being introduced into therapy of Cushing's disease and primary aldosteronism and being investigated in the treatment of low-renin essential hypertension. In adult male rats and in healthy, young, male volunteers the effect of trilostane on testosterone production was studied. Rats were treated with trilostane 150 mg or 300 mg/kg/d for 7 or 14 days. Testosterone in serum was measured by radioimmunoassay, testes were weighed and Leydig cell nuclear volume determined. In healthy volunteers, dehydroepiandrosterone sulphate (DHEAS) and responses of luteinizing hormone (LH), follicle stimulating hormone (FSH) and testosterone to luteinizing hormone releasing hormone (LHRH) stimulation were measured by radioimmunoassay before and during trilostane treatment (240 mg/d). In rats, trilostane treatment decreases testosterone and increases Leydig cell nuclear volumes without affecting testicular weight. In volunteers, basal testosterone is not changed during trilostane treatment but testosterone response to LHRH is impaired. DHEAS increases. LH or FSH levels are not altered. It is concluded that trilostane treatment may decrease testosterone synthesis.

Adult↗
PubMed1982

[A new test-strip for checking blood-sugar levels].

Blood sugar levels in 228 EDTA-treated venous blood samples were measured in the laboratory by a new test-strip (Visidex) and the hexokinase reference method. There was good agreement between the two, with a linear correlation of r = 0.92 and a regression line with a slope of 0.98. 97.8% of all values deviated by less than one concentration range from the reference values. At low glucose concentrations the median of the absolute differences between the two methods was 9.5 mg/dl. Over the whole concentration range of 20-800 mg/dl the mean deviation from the reference values was between 14.4 and 32.6 mg/dl. The results indicate that the Visidex test-strip method is suitable for the visual estimation of blood sugar values.

Blood Glucose↗
PubMed1982

[Various aspects of the regulation of aldosterone secretion].

Angiotensin was regarded as the major stimulus of aldosterone secretion until the late sixties, when the discussion about the regulation of aldosterone release has been renewed. The present study demonstrates the response of plasma renin activity, aldosterone in serum and electrolytes in serum and urine to ACTH (0.25 mg Synacthen i.v.), pretreatment with dexamethasone (2 mg Millicorten p.o.) and to combined administrations of furosemide (40 mg Lasix i.v.) + potassium (80 mmol Kalinor p.o.) and furosemide + propranolol (5 mg Dociton i.v.) in eight healthy volunteers. Plasma renin activity and aldosterone were measured by radioimmunoassay, electrolytes in serum and urine according to routine methods. ACTH increases aldosterone without influencing plasma renin activity. Pretreatment with dexamethasone decreases aldosterone and stimulates renin response to upright posture. Potassium delays the increase of plasma renin activity after furosemide and propranolol inhibits the furosemide-induced renin release, both without impairing aldosterone secretion. We conclude that the regulatory system of aldosterone production is far more complex than suggested by the concept of the renin-angiotensin-aldosterone-system.

Adrenocorticotropic Hormone↗