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Biomedical subjects

E Jungmann

Publications and source records attributed to E Jungmann.

At least 91 records · Page 5Linked to original sources
PubMed1988

Impaired renal responsiveness to human atrial natriuretic peptide (hANP) in normotensive patients with type 1 diabetes mellitus.

Potential impairment of the efficacy of human atrial natriuretic peptide (human ANF-(99-126), hANP), the most potent endogenous natriuretic agent in healthy subjects, was examined in eight male normotensive patients with uncomplicated type 1 diabetes mellitus (aged 22-37 years). After giving informed consent, patients and eight male control subjects (aged 22-28 years) received in a random double-blind study design i.v. bolus injections of 100 micrograms hANP (Bissendorf peptide) or placebo. At base-line, patients differed from controls in elevated creatinine clearance (P less than 0.05) and in mild postprandial hyperglycemia. Whereas the responses of urinary cyclic guanosine monophosphate, the second messenger of hANP, were found to be normal in patients, the diuretic and natriuretic effects of hANP were grossly impaired when compared to controls (P less than 0.01); hANP resulted in increased plasma protein concentrations only in controls (P less than 0.05 vs patients). In both groups, creatinine clearance remained uninfluenced by hANP. There were similar decreases in plasma renin activity, aldosterone, levels, and blood pressure (systolic more than diastolic) in both groups (P less than 0.05 vs placebo). Heart rate and blood glucose remained unchanged. Thus, there is evidence for a decreased responsiveness to hANP exclusively of renal fluid, sodium, and chloride excretion in uncomplicated type 1 diabetes mellitus. The mechanisms responsible for this phenomenon remain obscure, neither a down regulation at the hANP receptor sites nor an hANP-induced shift from intra- to extravascular fluid volume are likely to be involved in its probably diabetes-specific pathogenesis.

Adult↗
PubMed1988

[What pathophysiologic significance does increased plasma levels of human atrial natriuretic peptide have in patients with diabetes mellitus?].

Hypertension is more frequently found in patients with diabetes mellitus than in subjects with normal glucose tolerance. On the other hand, concomitant hypertension accelerates the progression of diabetic nephropathy. To examine whether human atrial natriuretic peptide (human ANF-[99-126], hANP) is involved into the pathogenesis of hypertension and nephropathy of diabetic patients and to find out whether the detection of increased hANP levels can serve as an early marker, helping to identify diabetic patients at increased risk of developing these diabetes complications, we studied 107 randomly selected patients with Type 1 or Type 2 diabetes mellitus (53 women, 54 men). There were no differences between patients with normal hANP levels and patients with hANP levels above normal range regarding age, diabetes duration, metabolic control, kidney function (creatinine clearance and proteinuria), electrolytes, and in plasma renin activity, aldosterone, epinephrine and norepinephrine levels in plasma. However, higher blood pressure was measured and antihypertensive therapy was found more frequently in patients with increased hANP levels (p less than 0.05). This was confirmed by analyzing the subgroup of patients with normal blood pressure without antihypertensive therapy: Again, diastolic blood pressure was found to be higher (p less than 0.05) in patients with elevated hANP than in patients with normal hANP levels. In this subgroup, increased creatinine clearance tended to be found more frequently among patients with increased hANP levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Natriuretic Factor↗
PubMed1988

Dopaminergic effects on kidney function and responsiveness of aldosterone, plasma renin activity, prolactin, catecholamines, and blood pressure to stimulation in patients with prolactinoma. Comparison of the efficacy of pergolide and bromocriptine therapy.

8 beta-[(Methylthio)methyl]-6-propylergoline (pergolide) is a new, potent, long-acting dopaminergic DA2 receptor agonist currently being investigated for therapeutic use in patients with hyperprolactinemia, acromegaly or Parkinsons's disease. Since the influence of bromocriptine, a well-established dopaminomimetic compound, on aldosterone responsiveness and plasma renin activity is still a matter of debate, the efficacies of both compounds on these parameters and on kidney function, blood pressure, catecholamine release and prolactin levels were compared in 16 patients with prolactinoma. Supine and furosemide (40 mg i.v.)-stimulated plasma renin activity and aldosterone levels were similarly decreased by bromocriptine (2.5-30 mg/d) and pergolide (50-500 micrograms/d). Suppression of blood pressure, inhibition of stimulated norepinephrine release, increase in creatinine clearance, and decrease in base-line prolactin levels were similarly pronounced during treatment with both compounds. Metoclopramide (10 mg i.v.)-induced stimulation of aldosterone and prolactin levels, however, were suppressed only by bromocriptine and not by pergolide. It remains to be studied whether this difference between bromocriptine and pergolide is due to a potential agonist effect of pergolide on dopaminergic DA1 receptors which are influenced by bromocriptine in an antagonistic manner, or whether pergolide can be more readily displaced from its receptors than bromocriptine.

Adult↗
PubMed1987

[Plasma renin activity and aldosterone behavior in critically ill patients].

To investigate the influence of critical illness on plasma renin activity and aldosterone levels and to examine potential inhibitory effects of dopamine therapy on aldosterone responsiveness, we measured plasma renin activity, and potassium and creatinine in serum, as well as the responses of aldosterone, cortisol and prolactin levels to TRH 200 micrograms i.v. + Synacthen 0.25 mg i.v. in 63 unselected, critically ill patients (32 females, 31 males, aged 18-84 years). Of the patients 19 received dopamine treatment (3-13 micrograms/kg/min i.v.); 21 of the patients died in the further course of their disease. Plasma renin activity was increased in 66.7% of the patients and aldosterone levels were elevated in 90.5% of the patients. There were correlations (P less than 0.05) of lethality with plasma renin activity and cortisol levels and correlations (P less than 0.01) of aldosterone concentrations with plasma renin activity and cortisol levels. Whereas dopamine treatment had no inhibitory effect on aldosterone levels before and after stimulation, prolactin stimulation was decreased in dopamine-treated patients. Thus, dopamine does not generally lose its potency of hormone inhibition in critically ill patients, but has no influence on the secondary aldosteronism developing regularly in the early phase of critical illness, which is apparently mainly due to the stimulatory effect of ACTH (or ACTH-related pituitary peptides) and is considered an epiphenomen of the stress mechanisms acting upon the patients in this condition.

Aldosterone↗
PubMed1987

Long-term treatment of severe chronic heart failure with captopril: a double-blind, randomized, placebo-controlled, long-term study.

Twenty-three patients with severe heart failure (NYHA classes III and IV) on treatment with digitalis and diuretics were additionally treated in a randomized double-blind study over a 6-month period with captopril (n = 12; mean daily dose 84 mg) or a placebo (n = 11) and were then reexamined. In the captopril group, the left-ventricular filling pressure decreased by 9 mm Hg (from 23 to 14) at rest and 6 mm Hg (from 35 to 29) during exercise. In the placebo group, there was an increase of 4 mm Hg (from 25 to 29) at rest and 7 mm Hg (from 33 to 40) during exercise; p less than 0.01 (p less than 0.01). In the captopril group, the cardiac index at rest increased 0.7 1/min/m2 (from 2.1 to 2.8) and during exercise 1.2 1/min/m2 (from 2.8 to 4.0). In the placebo group, the increase in cardiac index was considerably less pronounced at rest (= 0.2 1/min/m2; from 1.9 to 2.1) and during exercise (= 0.1 1/min/m2; from 2.7 to 2.8); p less than 0.02 (p less than 0.01). The improved cardiac output had a beneficial effect on the renal blood flow. Hippuran clearance increased by 46 ml/min (from 271 to 318), whereas in the control group it decreased 25 ml/min (from 259 to 234) (p less than 1.02). Both the heart rate and the arterial blood pressure remained constant, whereas the decrease in peripheral vascular resistance was definitely more pronounced in the captopril group (= 562 dyne X s X cm-5, from 1,841 to 1,279) than in the placebo group (= 123 dyne X s X cm-5, from 1,834 to 1,710; p less than 0.02). The heart volume, assessed radiographically, increased slightly in the placebo group, and the left-ventricular end-diastolic diameter remained constant in both groups. In the course of the study, two patients died in the captopril group and three in the placebo group. After six months, eight patients in the captopril group and three in the placebo group had improved by at least one NYHA category. The beneficial effects of captopril are due to its inhibitory effect on the renin-angiotensin system as well as to the inhibition of sympathetic stimulation. Consequently, in the captopril group the quantity of plasma norepinephrine decreased by 188 ng/ml (from 430 to 618); p less than 0.03. The indirect vasodilation caused by this mechanism leads to persistent unloading of the myocardium and an improvement in heart failure without loss of action by counterregulatory mechanisms.

Captopril↗
PubMed1986

The role of adrenal medulla in endogenous dopaminergic inhibition of aldosterone secretion.

Evidence has accumulated that aldosterone secretion is under endogenous dopaminergic inhibition. To examine potential sources of the dopamine thus inhibitorily acting in the adrenal zona glomerulosa, the responsiveness of aldosterone, plasma renin activity, prolactin, and plasma catecholamines to haloperidol, a dopaminergic antagonist, was studied in rats 6 weeks after unilateral adrenalectomy (Group B), 6 weeks after unilateral adrenal demedullation followed by contralateral adrenalectomy 5 days later (Group C), and in controls without any pretreatment (Group A). In Group C, there were increases in basal levels of norepinephrine (P less than 0.01), prolactin (P less than 0.02), and aldosterone (P less than 0.01). Basal plasma renin activity was also increased (P less than 0.05), epinephrine concentrations were decreased. Two hours after haloperidol 1 mg/kg b.wt. i.p., aldosterone levels were increased in Groups A + B (P less than 0.01) but unresponsive in Group C. Haloperidol-induced stimulation of prolactin and norepinephrine was not impaired by the surgical procedures. Epinephrine levels were increased by haloperidol only in groups A + B (P less than 0.002). In none of the groups were plasma renin activity or dopamine levels influenced by haloperidol. It is concluded that dopaminergic inhibition of aldosterone production is brought about neither by circulating dopamine nor by potential dopaminergic nerves accompanying arterial blood supply of the adrenal cortex but by dopamine originating directly in adrenal medulla.

Adrenal Medulla↗
PubMed1986

Endogenous dopaminergic inhibition of aldosterone and prolactin secretion is apparently not increased in primary aldosteronism.

To examine the previous suggestion that the endogenous dopaminergic activity would be increased in patients with primary aldosteronism, dose-response curves of aldosterone and prolactin stimulation by the dopamine antagonist metoclopramide were established in a pilot study by injecting metoclopramide 1, 2.5, and 10 mg i.v. consecutively at hourly intervals to 6 patients with primary aldosteronism and 14 healthy volunteers. All three metoclopramide doses induced clear-cut rises in aldosterone levels both in patients with primary aldosteronism and healthy controls. Basal aldosterone concentration was higher in range in the patients but the dose-response curves were nearly parallel one with the other. Prolactin responsiveness was also very similar. Thus, the present findings do not support the hypothesis of an increase in endogenous dopaminergic activity in primary aldosteronism.

Adult↗