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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 58 (1980), S. 185-194 
    ISSN: 1432-1440
    Keywords: Hypoaldosteronismus ; Diabetes mellitus ; Nierenerkrankung ; Hyperkaliämie ; Kalium ; Natrium ; Renin ; Hypoaldosteronism ; Diabetes mellitus ; Renal disease ; Hyperkalemia ; Potassium ; Sodium ; Renin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Selective hypoaldosteronism has almost invariably been described with hyperkalemia as principal manifestation. The prevalence of hypoaldosteronism and its relationship to plasma potassium, sodium, renin activity (PRA), body sodium-volume state and renal function was evaluated prospectively in 100 non-azotemic patients with diabetes mellitus and 46 with renal disease and normal to moderately impaired kidney function. Ninety healthy subjects served as controls and provided normal ranges for PRA and aldosterone (PA) relative to age and/or sodium excretion. Six diabetics (6%) and 2 renal patients (4.5%) had hypoaldosteronism; their plasma creatinine was 〈1.4 mg/100 ml. Nineteen diabetics (19%) and 13 renal patients (26%) had borderline hypoaldosteronism; 10 of the renal group had a plasma creatinine of 1.4 to 3.9 mg/100 ml. Plasma cortisol was consistently normal. Except for the presence of hyperkalemia in one patient with borderline hypoaldosteronism and azotemia, plasma potassium was also normal. Mean age, blood pressure, plasma cortisol and electrolytes, urinary potassium, blood glucose (diabetics only) and blood volume, exchangeable sodium and renal function were comparable between low, borderline-low or normal PA subgroups with diabetes or kidney disease. The body sodium-volume state was normal except for increased (p〈0.01) exchangeable sodium in diabetics. PA correlated (p〈0,01) with PRA. Mean PRA tended to be lowered in hypoaldosteronism; but some patients of this subgroup and most with borderline hypoaldosteronism had normal PRA. These findings demonstrate that hypoaldosteronism may exist without hyperkalemia or overt sodium wasting and may accompany non-azotemic diabetes mellitus or renal disease. This constellation favors a more facultative role of aldosterone as factor protecting against potassium retention in non-azotemic man. Asymptomatic hypoaldosteronism is probably more common than the symptomatic form and may be caused by angiotensin-deficiency or altered adrenal function.
    Notes: Zusammenfassung Der selektive Hypoaldosteronismus ist bisher fast ausschließlich mit Hyperkaliämie als Hauptmanifestation beschrieben worden. Bei 100 Patienten mit Diabetes mellitus und 46 Nierenkranken wurden prospektiv die Häufigkeit von Hypoaldosteronismus und dessen Beziehung zu Plasma-Kalium,-Natrium und -Reninaktivität, Körper-Natrium-Volumenstatus und Nierenfunktion untersucht. 90 Normalpersonen waren die Kontrollen und lieferten die Normbereiche für Plasma-Renin und -Aldosteron in Beziehung zum Alter und/oder Urinnatrium. 6 Diabetiker (6%) und 2 Nierenkranke (4,5%) hatten einen Hypoaldosteronismus; ihr Plasmakreatinin war normal (〈1,4 mg/100 ml). 19 Diabetiker (19%) und 13 Nierenkranke (26%) hatten einen grenzwertigen Hypoaldosteronismus; 10 der Nierenkranken hatten ein erhöhtes Plasma-Kreatinin (1,4–3,9 mg/100 ml). Plasma-Cortisol war immer normal. Außer einer Hyperkaliämie bei einem Patienten mit grenzwertigem Hypoaldosteronismus und Azotämie war das Plasmakalium ebenfalls normal. Mittleres Alter, Blutdruck, Plasma-Cortisol und -Elektrolyte, Urin-Kalium, Blutzucker (nur Diabetiker), Blutvolumen, und austauschbares Natrium waren bei Diabetikern oder Nierenkranken mit tiefem, normalem oder hohem Plasmaaldosteron vergleichbar. Plasma-Aldosteron korrelierte (P〈0,01) mit Plasma-Renin. Hypoaldosteronismus war mit einer Tendenz zu niedrigem Plasma-Renin assoziiert. Gewisse Patienten mit Hypoaldosteronismus und die meisten mit grenzwertigem Hypoaldosteronismus hatten jedoch normale Reninwerte. Diese Befunde belegen das Vorkommen von Hypoaldosteronismus ohne Hyperkaliämie oder manifestem, renalem Natriumverlust bei Patienten mit nichtazotämischen Diabetes oder Nierenkrankheit. Diese Konstellation spricht dafür, daß Aldosteron als protektiver Faktor gegen Kaliumretention beim nichtazotämischen Menschen eine fakultative Rolle spielt. Asymptomatischer Hypoaldosteronismus ist vermutlich häufiger als die symptomatische Form. Als Ursache kommen Reninmangel oder eine gestörte Nebennierenrindenfunktion in Frage.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Orale Glukose-Belastung ; Insulin ; Kalium ; Renin ; Aldosteron ; Oral glucose-load ; Insulin ; Potassium ; Renin ; Aldosterone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The effects of a standard oral glucose load (100 g) on plasma glucose, insulin, potassium, renin and aldosterone levels were investigated in 10 supine normal subjects (Group A). Responses of plasma glucose, insulin, potassium and aldosterone to glucose ingestion were evaluated further in 16 seated normal or borderline hypertensive subjects (Group B), studied in the untreated state as well as following renin-aldosterone activation by diuretic pre-treatment. In both groups, the increase in plasma glucose and insulin following glucose ingestion was accompanied by an acute decrease (p〈0.01) in plasma potassium and aldosterone levels, which in Group A was associated with an increase (p〈0.02) in plasma renin activity. In all subjects analyzed together, significant (p〈0.005) correlations were noted between plasma aldosterone and potassium levels and between glucose-induced changes in these factors. In Group A, there were significant (p〈0.001) correlations between glucose-induced changes in plasma aldosterone and renin values and between absolute aldosterone and renin levels in the glucose-loaded state. Plasma aldosterone or renin levels following glucose-load were unrelated to glucose or insulin values. These findings indicate that an oral standard glucose load causes acutely marked aldosterone suppression and mild but distinct renin stimulation. The glucose-induced inhibition of aldosterone secretion appears to depend on insulin-mediated changes in potassium metabolism and may be partly counteracted by concomitant renin activation.
    Notes: Zusammenfassung Der Einfluß einer oralen Standard-Glukosebelastung (100 g) auf die Plasma-Konzentrationen von Glukose, Insulin, Kalium, Renin und Aldosteron wurde bei 10 liegenden Normalpersonen untersucht (Gruppe A). Das Verhalten der Plasma-Konzentrationen von Glukose, Insulin, Kalium und Aldosteron nach einer solchen Glukose-Einnahme wurde zudem bei 16 sitzenden, normalen oder grenzwertig-hypertensiven Personen studiert (Gruppe B), wobei die Untersuchungen im unbehandelten Zustand sowie nach Aktivierung des Renin-Aldosteron-Systems durch Vorbehandlung mit Diuretika erfolgten. In beiden Gruppen wurde der Anstieg der Plasma-Glukose und -Insulinwerte nach Glukose-einnahme von einer akuten Senkung (p〈0,01) der Plasma-Kalium und -Aldosteron-Konzentrationen begleitet. In Gruppe A fand sich gleichzeitig ein signifikanter Anstieg (p〈0,02) der Plasma-Renin-Aktivität. Die gemeinsame Analyse aller Personen ergab signifikante (p〈0,005) Korrelationen zwischen den basalen (prä-Glukose-Infusion) Absolutwerten von Plasma-Aldosteron und -Kalium einerseits und zwischen den Glukose-induzierten Änderungen dieser beiden Parameter andererseits. In Gruppe A fanden sich zudem nach der Glukose-Einnahme signifikante Beziehungen zwischen den absoluten Plasma-Aldosteron und-Reninwerten, sowie zwischen den Änderungen dieser beiden Parameter (p〈0,001). Dagegen korrelierten Plasma-Aldosteron- oder -Reninspiegel nicht signifikant mit den Glukose- oder Insulinwerten. Diese Befunde zeigen, daß eine orale Standard-Zufuhr von Glukose akut eine markante Aldosteron-Hemmung und eine leichte, aber signifikante Renin-Stimulation bewirkt. Die Glukose-induzierte Aldosteron-Suppression scheint mit den Insulin-vermittelten Änderungen des Kaliummetabolismus in Zusammenhang zu stehen und durch die Renin-Aktivierung teilweise antagonisiert zu werden.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1440
    Keywords: Serum lipoproteins ; Diuretics ; Muzolimine ; Renal disease ; Hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Patients with renal functional impairment are prone to develop hypertension and hyperlipidemia, and both abnormalities tend to occur already at an early stage of kidney disease. In 18 patients with mild renal disease (glomerular filtration rate 65±5 ml/min) and hypertension (mean blood pressure 126±4 mm Hg), the effect of six weeks of treatment with the loop-diuretic muzolimine on serum lipoproteins was assessed. Compared to placebo values, the diuretic significantly increased serum low-density lipoprotein cholesterol (LDL-C) and apoprotein B (+18 and 11%, respectively,P〈0.005) in 13 men or postmenopausal women, but not in 5 premenopausal women. Serum high-density lipoprotein cholesterol (HDL-C), and total triglycerides or lipoprotein triglyceride fractions were not consistently changed in both subgroups. Thus, the ratio LDL-C/HDL-C was increased from 3.2±0.3 to 3.9±0.3 (P〈0.05) in the men or postmenopausal women, while no such tendency occurred in the premenopausal women (4.1±0.6 to 3.7±0.6). Changes in serum LDL-C were not associated with hemoconcentration or alterations in carbohydrate metabolism and were not related to variations in serum potassium or blood pressure. Increased serum levels of the atherogenic LDL-C fraction during diuretic treatement in men or postmenopausal women with renal disease may represent a potentially undesirable effect, particularly since such patients may tend to have hyperlipidemia in the untreated state.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-1440
    Keywords: Aldosterone ; Glucose ; Insulin ; Potassium ; Renin-angiotensin system ; Cortisol ; Captopril
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucose loading is known to cause acute suppression of plasma aldosterone and stimulation of plasma renin activity. The relative contribution of variations in circulating angiotensin II to the regulation of aldosterone secretion following glucose loading was assessed in ten normal subjects. The effects of a standard oral glucose loading test (100 g) on plasma concentrations of glucose, insulin, potassium, aldosterone, renin activity and cortisol were studied (a) under basal conditions, and (b) after inhibition of angiotensin II with the converting enzyme inhibitor captopril (50 mg t.i.d. during 3 days). Under basal conditions the acute increase in plasma glucose and insulin after glucose loading was accompanied by a significant decrease (P〈0.01) in plasma cortisol and aldosterone and by a significant increase in plasma renin activity (P〈0.01); plasma potassium was decreased slightly but not significantly. Following captopril treatment preloading plasma renin activity was increased significantly, most probably reflecting an effective reduction of angiotensin II. Glucose loading caused a similar suppression of plasma aldosterone, as observed under basal conditions. This observation suggests that renin activation does not substantially contribute to the acute regulation of plasma aldosterone after an oral glucose load.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1041
    Keywords: Angiotensin-converting enzyme inhibitor ; Lisinopril ; Hypertension ; Insulin sensitivity ; Lipoprotein metabolism ; physical fitness
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Abstract To investigate the effects of antihypertensive treatment with the angiotensin-converting enzyme (ACE) inhibitor lisinopril on insulin sensitivity and related metabolic variables, the insulin sensitivity index (SI), determined with the Minimal Model Method of Bergman, fasting plasma insulin and glucose concentrations, serum total triglyceride and lipoprotein cholesterol fractions, and blood pressure were assessed in 24 lean, non-diabetic patients with essential hypertension. Following a double-blind, randomised crossover design, these parameters were measured after a 4-week run-in period, after 8 weeks of lisinopril or placebo, and after an additional 8 weeks on placebo or lisinopril, respectively. Furthermore, the level of physical fitness was estimated using the Conconi bicycle ergometer test. SI was low in this study population (5.6 vs 13.3 · 10−4·min−1·mU−1·1−1 in normal lean control subjects). It did not differ between the placebo run-in phase, the lisinopril phase, and the placebo crossover phase (5.8, 5.5, and 5.4·10−4·min−1·mU−1·1−1, respectively). Moreover, during the administration of lisinopril, no significant changes occurred in fasting plasma insulin and glucose, areas under the glucose and insulin curves, glucose disappearance rate, serum total triglycerides, and cholesterol or lipoprotein cholesterol fractions. Heart rate at rest, body weight, and anaerobic threshold remained stable throughout the study. Compliance assessed by pill-counting exceeded 90% at all visits. These findings demonstrate that the ACE inhibitor lisinopril is neutral with regard to insulin sensitivity, plasma insulin and glucose, and lipoprotein metabolism in patients with essential hypertension.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 555-560 
    ISSN: 1432-1440
    Keywords: Diabetes mellitus ; Plasma norepinephrine ; Norepinephrine clearance ; Hypertension ; Diabetes Mellitus ; Plasmanoradrenalin ; Noradrenalin-Clearance ; Hypertonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 27 Patienten mit nicht-azotämischem Diabetes mellitus und 27 Normalpersonen wurde unter einer konstanten Noradrenalin-Infusion bei zwei verschiedenen Infusionsraten die Gesamt-Plasmaclearance von Noradrenalin gemessen. Um vergleichbare Blutdruckerhöhungen zu erzeugen, waren bei Diabetikern niedrigere Noradrenalindosierungen notwendig als bei Normalpersonen. Dabei fand sich bei beiden Gruppen eine gleichartige Beziehung zwischen den Noradrenalininfusionsraten und den gleichzeitig gemessenen Plasmanoradrenalinspiegeln (r=0,79 und 0,78;P〈0,001). Die Plasma-Noradrenalinclearance war bei niedrigeren und höheren Noradrenalin-Infusionsraten bei Diabetikern und Normalpersonen vergleichbar (6,0±3,1 und 5,1±2,6 1/min). Außerdem korrelierte die Plasmaclearance von Noradrenalin in beiden Gruppen negativ mit der basalen Plasmanoradrenalinkonzentration (r−=0,38 und −0,53;P〈0,05). Schließlich fanden sich auch zwischen 13 Diabetikern ohne und 14 mit Zeichen von peripherer Neuropathie bzw. zwischen 17 Diabetikern mit normalem und 10 mit erhöhtem Blutdruck keine signifikanten Unterschiede in der Beziehung zwischen Noradrenalin-Infusionsraten und Plasmanoradrenalin oder in der Plasmaclearance von Noradrenalin. Diese Ergebnisse weisen darauf hin, daß die Kinetik von zirkulierendem Noradrenalin bei nicht-azotämischem Diabetes mellitus meistens unverändert ist. Bei solchen Patienten könnte eine gesteigerte Pressorreaktivität gegenüber Noradrenalin in Gegenwart von normalen Plasmanoradrenalinkonzentrationen ein prädisponierender Faktor für die Entwicklung eines Hochdrucks sein.
    Notes: Summary The total plasma clearance of norepinephrine (NE) was assessed during steady state NE infusion at two different dose rates in 27 patients with non-azotemic diabetes mellitus as compared with 27 normal subjects. Lower NE dose rates were required in diabetics than in normal subjects (P〈0.001) to induce similar increases in blood pressure. However, plasma NE levels during NE infusion correlated closely (r=0.79 and 0.78;P〈0.001) with concomitant dose rates, and this relationship was similar in both study groups. Moreover, the plasma NE clearance did not differ between low and high dose rates of NE infusion, and was similar in diabetics and normal subjects (6.0±3.1 and 5.1±2.6 liter/min, respectively). It correlated inversely with the pre-infusion plasma NE (r=−0.38 and −0.53;P〈0.05); this relationship was also similar in the two groups. The correlation relating plasma NE to NE infusion rates as well as the plasma NE clearance did not differ between the 13 diabetics without and the 14 with signs of peripheral neuropathy or between the 17 patients with normal and the 10 patients with high blood pressure. These findings suggest that the kinetics of circulating NE are usually unaltered in non-azotemic diabetes mellitus. An increased pressor responsiveness to NE, in the presence of normal plasma NE concentrations and clearance rates, may be a setting predisposing for the development of hypertension in diabetic patients.
    Type of Medium: Electronic Resource
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