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  • 1
    ISSN: 1432-1041
    Keywords: Nitrendipine ; Hypertension ; pharmacokinetics ; renal function ; hypertensive crisis ; pharmacodynamics ; blood pressure ; adverse effects
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Nitrendipine solution 5 mg·ml−1 in the dose of 5 mg was given orally to 20 patients with chronic renal failure and elevated diastolic blood pressure (≥110 mmHg), of whom 10 were on maintenance haemodialysis (endogenous creatinine clearance 〈5 ml·min−1) and 10 were at the predialysis stage (endogenous creatinine clearance 5–20 ml·min−1). The aim of the study was to investigate the influence of kidney function and/or dialysis treatment on the pharmacokinetic and pharmacodynamic profile of a solution of nitrendipine and to assess its antihypertensive efficacy. After 10 min there was a significant reduction in blood pressure from 188/113 to 173/100 (patients not dependent on dialysis) and from 197/112 to 161/94 mmHg (patients dependent on dialysis). The maximum fall in blood pressure (approximately 30%) was attained after 90 min in the dialysis patients and after 120 min in the non-dialysis group. Blood pressure increased again about 3 h after the administration of nitrendipine but it was still below baseline after 12 h. The terminal elimination half-life (4.1 h in the dialysis patients and 3.6 h in non-dialysis patients) was similar to that observed in patients with normal renal function. The pharmacokinetics of nitrendipine did not differ between the dialysis and non-dialysis groups. There was a correlation between plasma concentration and the blood pressure reduction. The maximum plasma concentration of nitrendipine was reached after 0.5 h (median) and did not differ between the two groups. The mean maximum plasma concentration was 14.8 μg·1−1 in the study population as a whole, with comparable means in the dialysis (17.3 μg·1−1) and non-dialysis (12.4 μg·1−1) groups. The nitrendipine solution proved to be effective in lowering acutely elevated blood pressure in patients with advanced renal failure and renal hypertension, and was well tolerated. The pharmacokinetics was not affected by renal impairment or by dialysis.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Adrenaline ; Noradrenaline ; Adrenal medulla ; Pheochromocytoma ; Hypertension ; Adrenalin ; Noradrenalin ; Nebennierenmark ; Phäochromozytom ; Hypertonie
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Bei 10 Personen (5 mit normalem Blutdruck, 4 mit essentieller Hypertonie, 1 mit renaler Hypertonie) wurden die lokalen Katecholaminkon-zentrationen im Blut der Vena suprarenalis, Vena renalis, Vena cava inferior und Vena iliaca mit einer radioenzymatischen Methode bestimmt. Es fanden sich folgende Konzentrationen pro Milliliter Plasma: (1) In der Vena suprarenalis der linken Nebenniere 13,87±8,18 ng Adrenalin und 2,82±1,82 ng Noradrenalin; (2) in der Vena renalis, nach der Mischung mit dem Blut der einströmenden Vena suprarenalis, 1,44±1,13 ng Adrenalin und 0,37±0,18 ng Noradrenalin; (3) in der Vena cava inferior, cranial der Nierenvenenzuflüsse, 0,16±0,10 ng Adrenalin und 0,30±0,10 ng Noradrenalin; (4) in der Kreislaufperipherie, zum Beispiel im Blut der Vena iliaca, betrug die Adrenalinkonzentration mit 0,09±0,03 ng nur noch 1/154 der ursprünglichen Konzentration im Nebennierenvenenblut, die Noradrenalinkonzentration lag hier bei 0,24±0,14 ng/ml Plasma. Unter der Annahme, daß das vom Nebennierenmark freigesetzte Noradrenalin den gleichen Verteilungs- und Eliminationsmechanismen wie Adrenalin unterliegt, wurde errechnet, daß unter basalen Sekretionsbedingungen im Durchschnitt nur 7,5% des in der Kreislaufperipherie zirkulierenden Noradrenalins aus dem Nebennierenmark stammen. Die Adrenalin- und Noradrenalinkonzentration im Nebennierenvenenblut bei Patienten mit essentieller Hypertonie war nicht höher als bei Personen mit normalem Blutdruck.
    Notes: Summary In 10 human subjects (5 with normal blood pressure, 4 with essential hypertension, 1 with renal hypertension) local catecholamine levels in blood of suprarenal vein, renal vein, inferior vena cava and iliac vein were determined by a radioenzymatical method. The following concentrations per ml plasma were found: (1) in the suprarenal vein of the left adrenal gland 13.87±8.18 ng adrenaline and 2.82±1.82 ng noradrenaline; (2) in the left renal vein, after confluence of suprarenal with renal blood, 1.44±1.13 ng adrenaline and 0.37±0.18 ng noradrenaline; (3) in the inferior vena cava, cranial of both renal veins, 0.16±0.10 ng adrenaline and 0.30±0.10 ng noradrenaline; (4) in periphery, as in the iliac vein, the plasma adrenaline concentration was only 0.09±0.03 ng/ml, corresponding to 1/154 of suprarenal vein blood concentration; the noradrenaline concentration in iliac vein was 0.24±0.14 ng/ml plasma. Assuming that noradrenaline released from the adrenal medulla follows the same distribution and elimination mechanisms as adrenaline, it was calculated that only 7.5% of noradrenaline found under basal conditions in the periphery of the circulation, originates from the adrenal medulla. The adrenaline and noradrenaline concentration in blood of suprarenal vein of patients with essential hypertension was not higher than the concentrations found in subjects with normal blood pressure.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Clinical and experimental medicine 152 (1970), S. 306-312 
    ISSN: 1591-9528
    Keywords: Angiotensin ; Hypertension ; Adrenal glands ; Sodium content of the vascular wall ; Electrolytes ; Angiotensin ; Hypertonie ; Nebennieren ; Natriumgehalt der Gefäßwand ; Elektrolyte
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Durch Angiotensin II-Infusionen über mehrere Tage konnte bei Ratten eine permanente Hypertonie hervorgerufen werden. Eine sekundäre „hypertensive Angiopathie“ in den Nieren zur Erklärung der chronischen Hypertonie wurde nicht festgestellt. Natrium und Kalium waren unmittelbar nach der Infusionsperiode in der Aortenwand erhöht. Gleichzeitig bestand eine Nebennierenhypertrophie. 3–4 Wochen nach Ende der Infusionsperiode war trotz Weiterbestehens der arteriellen Hypertonie das Natrium in der Aortenwand wieder normal oder leicht erniedrigt, ebenso nach 7–8 Wochen. Zu dieser Zeit hatte sich auch die Nebennierenhypertrophie zurückgebildet. Es ergibt sich die Hypothese, daß im Tierversuch eine renale Hypertonie möglicherweise durch eine zunächst erhöhte Aktivität des Renin-Angiotensin-Systems induziert wird. Diese Hypertonie verselbständigt sich und bleibt bestehen, auch wenn der anfänglich humorale Trigger-Mechanismus nicht mehr wirksam ist.
    Notes: Summary Infusions with Angiotensin II which were continued for several days resulted in a permanent hypertension with rats. A secondary “hypertensive angiopathy” in the kidneys explaining the chronic hypertension could not be found. Sodium and potassium were increased in the wall of the aorta immediately following the period of infusion. At the same time a suprarenal hypertrophy was ascertained. 3 to 4 weeks after the period of infusion and in spite of the continuance of the arterial hypertension the sodium content in the wall of the aorta was again back to normal or slightly reduced, similarly after 7 to 8 weeks. By that time also the suprarenal hypertrophy had receded. Thus the hypothesis arises that in animal experiments a renal hypertension may be induced by an initially increased activity of the Renin-Angiotensin system. This hypertension is rendered independent and continues to exist even after the initially humeral trigger mechanism is no longer effective.
    Type of Medium: Electronic Resource
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