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  • 1
    Electronic Resource
    Electronic Resource
    Verhalten der Plasmareninaktivität unter Langzeitbehandlung des Hochdrucks mit Propranolol (1977)
    Springer
    Journal of molecular medicine 55 (1977), S. 351-353 
    Details
    ISSN: 1432-1440
    Keywords: Plasma renin activity ; Long-term treatment ; Propranolol ; Essential hypertension ; Propranolol ; Essentielle Hypertonie ; Plasmareninaktivität ; Langzeitbehandlung
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung 17 Patienten im Alter von 40±9 Jahren mit essentieller Hypertonie wurden mit Propranolol als Monotherapie oral in Dosen von 120, 160 oder 240 mg pro die behandelt. Nach 4wöchiger Behandlung konnten der Blutdruck und die Herzfrequenz statistisch signifikant gesenkt werden und blieben auch bei Fortsetzung der Therapie nach insgesamt 6 Monaten unverändert. Die Plasmareninaktivität betrug vor Behandlungsbeginn 5,7±6,3 ng/ml/h und sank nach 4wöchiger Behandlung auf 1,8±1,3 ng/ml/h ab. 5 Monate später stieg das Plasmarenin im Durchschnitt wieder auf 5,0±0,9 ng/ml/h an. Der erneute Anstieg war ebenfalls statistisch signifikant zu sichern. Von den 17 Patienten hatten nach 6 monatiger Therapie noch 7 (41%) eine niedrigere Plasmareninaktivität als vor Behandlungsbeginn. Davon lagen aber nur 3 (18%) unter dem Wert, der nach 4wöchiger Behandlungsdauer bestimmt wurde. Aus den genannten Befunden wird geschlossen, daß der Wiederanstieg der Plasmareninaktivität möglicherweise ein reaktiver Mechanismus auf die langzeitige Blutdrucksenkung ist. Die Erniedrigung der Plasmareninaktivität nach Kurzzeitbehandlung mit Propranolol kann nicht als ein Mechanismus für den antihypertensiven Effekt dieses Medikaments bei der Langzeitbehandlung angesehen werden.
    Notes: Summary 17 patients (40±9 years) with essential hypertension were included in the study. A monotherapy of 120, 160 or 240 mg propranolol per day was administered orally according to the antihypertensive effect. Four weeks after treatment, blood pressure and heart rate showed a statistically significant decrease and remained unchanged over a period of six months. Plasma renin activity decreased significantly from 5.7±6.3 ng/ml/h at the beginning of the study to 1.8±1.3 ng/ml/h after 4 weeks. 5 months later however plasma renin activity increased again to 5.0±0.9 ng/ml/h. The difference was statistically significant. From 17 patients 7 (41%) had lower levels of plasma renin activity after 6 months treatment when compared with pretreatment values. In only 3 patients (18%) was plasma renin activity lower after 6 months than after four weeks. We conclude that the increase in plasma renin activity is a reactive mechanism to the reduced blood pressure under long-term conditions. The decrease of plasma renin activity in short-term treatment of essential hypertension is not a mechanism responsible for the antihypertensive effect of propranolol during long-term treatment.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01488116
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  • 2
    Electronic Resource
    Electronic Resource
    Arachidonic acid metabolites, hypertension and arteriosclerosis (1982)
    Springer
    Journal of molecular medicine 60 (1982), S. 479-488 
    Details
    ISSN: 1432-1440
    Keywords: Prostaglandins ; Hypertension ; Kidney ; Platelets ; Arteriosclerosis ; Prostaglandine ; Hypertonie ; Niere ; Thrombozyten ; Arteriosklerose
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Blutdruckhöhe wird durch komplexe Wechselwirkungen verschiedener Mechanismen bestimmt, die sowohl den Blutfluß als auch den Widerstand des Gefäßsystems beeinflussen. Ein Übergewicht der Faktoren, die den Gefäßwiderstand oder das Extrazellulärvolumen vergrößern, führt zu einem Anstieg des Blutdrucks. Solch ein Ungleichgewicht kann z.B. durch eine erhöhte Aktivität des sympathischen Nervensystems und des Renin-Angiotensin-Systems oder durch eine gesteigerte Mineralocorticoid-Sekretion verursacht sein. Ebenso könnte eine verminderte Aktivität blutdrucksenkender Faktoren wie der Prostaglandine oder des Kallikrein-Kinin-Systems zu einem Anstieg des Blutdrucks führen. In dieser Arbeit wird die mögliche Rolle der Prostaglandine für die Pathophysiologie der essentiellen Hypertonie und degenerativer Gefäßerkrankungen dargestellt, basierend auf der Beteiligung von Prostaglandinen an der Kontrolle des Gefäßwiderstandes, der renalen Regulation des Extrazellulärvolumens und der Thrombozyten-Gefäßwand-Wechselwirkung. Ein Ungleichgewicht der Synthese bestimmter Prostaglandin-Endoperoxid-Metabolite könnte zur Hochdruckentstehung beitragen, auch ohne Vorliegen einer erhöhten Aktivität der bekannten blutdrucksteigernden Faktoren. Dabei könnte die Beteiligung der Prostaglandine an der Entstehung von Hochdruck und degenerativer Gefäßerkrankung sowohl auf einer primären Abnormalität beruhen als auch in einer Mittlerrolle für bekannte Risikofaktoren wie hohe Kochsalz-und Fettzufuhr bestehen. Spezifische Blockade oder Stimulation bestimmter Biosynthesewege, die zu gegensätzlich wirksamen Prostaglandinen führen, oder Änderung der nutritiven Zufuhr von Prekursor-Fettsäuren sollte zu einem besseren Verständnis zugrunde liegender Pathomechanismen und zu neuen Ansatzpunkten für Therapie oder Prävention dieser Herz-Kreislauferkrankungen führen.
    Notes: Summary The level of arterial blood pressure is set by complex interactions of several mechanisms which influence both blood flow in and resistance of the vascular system. An imbalance favouring elevation of vascular resistance or extracellular volume will result in hypertension. Such alterations may include increased activity of the sympathetic nervous system, of the renin-angiotensin system, or excessive secretion of mineralocorticoids. Of equal importance may be a reduced activity of blood pressure-lowering factors such as prostaglandins and the kallikrein-kinin system. This paper describes the possible significance of prostaglandins in the pathophysiology of hypertension and in degenerative vascular disease, based on their involvement in the control of vascular resistance, renal regulation of extracellular volume and plateletvessel wall interactions. An abnormality in the biosynthesis of certain prostaglandin endoperoxide metabolites may lead to hypertension even without an increase in the activity of the classic blood-pressure-elevating systems. The contribution of prostaglandins for the development of hypertension and degenerative vascular disease may be based on an inherent abnormality of the prostaglandin system, as well as on the effects of major risk factors such as dietary intake of sodium and fat on prostaglandin synthesis. Specific blockade or stimulation of distinct biosynthetic pathways leading to antagonistically acting prostaglandins and nutritional manipulation of precursor fatty acids should lead to a better understanding of the pathomechanisms involved and may offer new strategies for therapy or prevention of these cardiovascular disorders.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01756093
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  • 3
    Electronic Resource
    Electronic Resource
    Rapid increase of mineralocorticoids after furosemide in low-renin essential hypertension: Evidence for 18-hydroxycorticosterone to be a better marker than aldosterone (1982)
    Springer
    Journal of molecular medicine 60 (1982), S. 847-852 
    Details
    ISSN: 1432-1440
    Keywords: Low-renin essential hypertension ; Furosemide ; Plasma renin activity ; Aldosterone ; 18-Hydroxycorticosterone ; Low-renin Hypertonie ; Furosemid ; Plasmareninaktivität ; Aldosteron ; 18-Hydroxycorticosteron
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Das Verhalten der Plasmareninaktivität (PRA), des Plasmaaldosterons, des 18-Hydroxycorticosterons (18-OH-B), des 18-Hydroxydeoxycorticosterons (18-OH-DOC) und des Corticosterons wurde nach Furosemid an 20 Normalpersonen, 16 Patienten mit normal-renin Hypertonie (NREH) und 12 Patienten mit low-renin Hypertonie (LREH) untersucht. Die Blutentnahmen erfolgten unmittelbar vor der Gabe von 40 mg Furosemid i.v. sowie 15 min (im Liegen) und 120 min (aktive Orthostase) danach. Die Normalpersonen zeigten 15 min nach Furosemid einen Anstieg der PRA von 0,8±0,4 ng AI/ml·min (SD) auf 3,4±1,4 (P〈0,01), des Plasmaaldosterons von 109±28 pg/ml auf 139±40 (P〈0,01) und des 18-OH-B von 199±90 pg/ml auf 279±85 (P〈0,01). Bei Patienten mit NREH stieg die PRA signifikant geringer an (P〈0,01). Dementsprechend wurde kein signifikanter Anstieg des Plasmaaldosterons und des 18-OH-B gefunden. Bei Patienten mit LREH blieb die PRA (basal 0,2±0,1) 15 min nach Furosemid praktisch unverändert. Das Plasmaaldosteron jedoch stieg von 111±37 auf 160±66 (P〈0,05) und das 18-OH-B von 162±101 auf 261±71 an (P〈0,01). Der relative Anstieg des 18-OH-B bei Patienten mit LREH war im Vergleich zu Patienten mit NREH signifikant höher. 120 min nach Furosemid lagen die Plasmaspiegel des Aldosterons und des 18-OH-B bei Normalpersonen signifikant höher als in den beiden Patientengruppen (P〈0,01). Die Corticosteron und 18-OH-DOC Plasmaspiegel zeigten zwischen den untersuchten Gruppen kein differentes Verhalten, und es fand sich nur 120 min nach Furosemid in Kombination mit aktiver Orthostase ein signifikanter Anstieg. Die Ergebnisse zeigen, daß die Sekretion der Mineralcorticoide bei Patienten mit LREH unmittelbar nach Furosemid gesteigert ist, obwohl die PRA unverändert bleibt. 18-OH-B ist anscheinend für dieses Phänomen ein empfindlicherer Index als Aldosteron.
    Notes: Summary The response of plasma renin activity (PRA), plasma aldosterone, 18-hydroxycorticoster-one (18-OH-B), 18-hydroxydeoxycorticosterone (18-OH-DOC) and corticosterone to furosemide were compared in 20 normal control subjects, 16 patients with normal-renin essential hypertension (NREH) and 12 patients with low-renin essential hypertension (LREH). Analyses were performed before medication, and 15 min (supine) and 120 min (active orthostasis) after IV administration of 40 mg furosemide. In normotensive subjects PRA increased 15 min after administration of furosemide from 0.8±0.4 ng AI/ml·h (SD) to 3.4±1.4 (P〈0.01), plasma aldosterone from 109±28 pg/ml to 139±40 (P〈0.01) and 18-OH-B from 199±90 to 279±85 (P〈0.01). In patients with NREH, PRA increased significantly less (P〈0.01) and no significant increase of plasma aldosterone or 18-OH-B was found. PRA of patients with LREH (0.2±0.1 ng AI/ml·h) remained practically unchanged 15 min after furosemide administration, but in contrast to NREH aldosterone increased from 111±37 to 160±66 (P〈0.05) and 18-OH-B from 162±101 to 261±71 pg/ml (P〈0.01). The relative increase of plasma 18-OH-B was significantly greater in patients with LREH than in patients with NREH. The plasma levels of aldosterone and 18-OH-B 120 min after furosemide administration were significantly higher in normotensive subjects than in either hypertensive group (P〈0.01). Corticosterone and 18-OH-DOC levels were the same in all investigated groups and increased significantly (P〈0.01) only at 120 min after furosemide administration combined with active orthostasis. In summary, our results support the concept that sensitivity of the mineralocorticoid-producing cells is enhanced in patients with LREH. Postfurosemide 18-OH-B seems to be a better marker of this phenomenon than aldosterone.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01728351
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  • 4
    Electronic Resource
    Electronic Resource
    Clinical and biochemical features of patients with aldosterone-producing adenoma and idiopathic hyperaldosteronism (1983)
    Springer
    Journal of molecular medicine 61 (1983), S. 35-42 
    Details
    ISSN: 1432-1440
    Keywords: Primary aldosteronism ; 18-Hydroxycorticosterone ; 18-Hydroxydeoxycorticosterone ; Saline infusion ; Angiotensin II ; Metoclopramide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Eight patients with aldosterone-producing adenoma (APA) (7 histologically proved) and 6 patients with idiopathic hyperaldosteronism (IHA) (2 histologically proved) were evaluated for differential diagnosis using clinical, radiographic, and biochemical parameters. Mean basal plasma aldosterone (445±146 (SD) pg/ml), 18-hydroxycorticosterone (975±394 pg/ml), and 18-hydroxydeoxycorticosterone levels (374±266 pg/ml) and mean diastolic blood pressure were significantly higher in patients with APA (p〈0.05 andp〈0.01), whereas mean plasma potassium levels and stimulated plasma renin activity were lower in subjects with APA as compared to patients with IHA (p〈0.01 andp〈0.01). Radiographic procedures predicted the correct diagnosis in 3 of 8 operated cases (37%) and selective adrenal vein sampling in 5 of 6 cases (83%). Urinary aldosterone excretion (30±10 µg/24 h) was suppressed inall patients with IHA after a 21 isotonic saline infusion in 2 h (13±6,p〈0.01). Inall patients with APA, however, aldosterone excretion wasnot suppressible (basal: 36±12). Plasma aldosterone levels of some patients with APA could be reduced by saline infusion and the response was not characteristically different between both groups. After 10 mg metoclopramide iv. the slopes of plasma aldosterone levels were similar for patients with APA and normal subjects. Patients with IHA showed a different secretion pattern with a delay of both the increase and the decline of aldosterone levels. Graded angiotensin II infusions (subpressor doses for normotensive individuals) did not increase plasma aldosterone levels in patients with APA. However, in patients with IHA, excessive increases of aldosterone levels were seen (basal: 268±54 pg/ml, after 4 ng A II/kg−1·min−1: 806±262). From these data, we conclude that patients with APA could be reliably identified before operation by determination of urinary aldosterone before and after a simple saline infusion test. Additionally, plasma aldosterone levels after metoclopramide iv. or angiotensin II infusions may be helpful diagnostic tools.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01484437
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  • 5
    Electronic Resource
    Electronic Resource
    Aldosterone 18-glucuronide excretion determined with and without chromatography in human hypertensives (1979)
    Springer
    Journal of molecular medicine 57 (1979), S. 1133-1135 
    Details
    ISSN: 1432-1440
    Keywords: Aldosteron-18-Glucuronid ; RIA mit und ohne Chromatographie ; Essentielle Hypertonie ; Aldosterone-18-glucuronide ; RIA with and without chromatography ; Essential hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary 24 h-urine excretion of aldosterone-18-glucuronide was determined with and without preceding paper chromatography in patients with essential hypertension (n=50). Radioimmunoassay was performed with a highly specific antibody against aldosterone. Urine specimens determined without chromatography gave significantly higher values than aliquots which were estimated at the same time with chromatography. A highly significant correlation was found between the two methods (r=0.91,p〈0.0001). Without chromatography, mean over estimation in samples with concentrations in the low and middle range was on average 32 and 24% respectively, whereas aldosterone concentrations in the upper range showed a 14% over estimation. The RIA procedure for aldosterone without chromatography as here described is suitable for hypertension screening programmes to exclude known forms of primary hyperaldosteronism in which elevated aldosterone excretion rates have to be differentiated from values lying within the normal range.
    Notes: Zusammenfassung Es wurde die Aldosteron-18-Glucuronidausscheidung im 24 h-Urin von essentiellen Hypertonikern (n=50) mit und ohne vorhergehender Papierchromatographie beschrieben. Der Radioimmunoassay wurde mit einem hochspezifischen Aldosteronantikörper durchgeführt. Die ohne Chromatographie analysierten Urine lagen signifikant höher als die dazu parallel bestimmten Proben mit Chromatographie (p〈0,02). Es konnte jedoch eine hochsignifikante Korrelation zwischen den beiden Methoden nachgewiesen werden (r=0,91,p〈0,0001). In Bereichen niederer und mittlerer Konzentrationen lagen die ohne Chromatographie bestimmten Proben in Mittel um 32 bzw. 24% über denen mit Chromatographie analysierten; Aldosteronkonzentrationen im Bereich der oberen Norm ergaben ohne chromatographisches Verfahren durchschnittlich um 14% höhere Werte. Die beschriebene Methode zur Bestimmung der Aldosteronexkretion ohne Chromatographie erscheint zur Abklärung von Hypertonikern geeignet, bei denen primäre Formen des Hyperaldosteronismus von normaler bzw. hoch normaler Aldosteronsekretion differenziert werden müssen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01481495
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  • 6
    Electronic Resource
    Electronic Resource
    Relief from malignant hypertension by treatment with captopril in a patient on maintenance hemodialysis (1980)
    Springer
    Journal of molecular medicine 58 (1980), S. 871-873 
    Details
    ISSN: 1432-1440
    Keywords: Maligne Hypertonie ; Dialysepatient ; Captopril ; Malignant hypertension ; Maintenance hemodialysis ; Captopril
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary A patient with end-stage renal disease due to malignant hypertension is described. Hypertension was resistant to hemodialysis. The orally active inhibitor of angiotensin-converting enzyme captopril (SQ 14.255; 2-D-methyl-3-mercaptopropanoyl-L-protein) dramatically lowered the elevated blood pressure both under ambulatory and dialysis conditions. No side effects were observed after 6 months' treatment. The effect of captopril could be described as a “biochemical nephrectomy”.
    Notes: Zusammenfassung Es wird ein Patient mit chronischem Nierenversagen auf dem Boden einer malignen Hypertonie beschrieben. Durch Dialysebehandlung konnte die Hypertonie nicht beherrscht werden. Der orale Angiotensin-converting Enzym Hemmstoff Captopril (SQ 14.255; 2-D-methyl-3-mercaptopropanoyl-L-prolin) erzielte eine dramatische Senkung des Blutdrucks sowohl unter ambulanten Bedingungen, als auch während der Dialyse. Nach 6 monatiger Behandlungsdauer wurden keine unerwünschten Wirkungen beobachtet. Die Wirkung von Captopril kann als „biochemische Nephrektomie“ beschrieben werden.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01476998
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  • 7
    Electronic Resource
    Electronic Resource
    Prostaglandin excretion after furosemide in normal and low-renin essential hypertension (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 777-782 
    Details
    ISSN: 1432-1440
    Keywords: Prostaglandins ; Furosemide ; Renin ; Potassium ; Kidney function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We examined the urinary excretion of prostaglandin (PG)E2 and PGF2α before and 15 min after stimulation with the acutely vasodilating agent furosemide in 25 normotensive controls and 81 patients with essential hypertension (EH). After furosemide administration, PGE2 excretion was lower in patients with EH (P〈0.02). Excretion rates of PGF2α and of sodium, and urinary volume in hypertensive patients were not significantly different from the values found in normotensive controls. Patients with low-renin essential hypertension (LREH) had a significantly reduced excretion of both PGE2 and PGF2α before and after administration of furosemide as compared to controls. The difference in PGF2α excretion was also significant when LREH patients were compared to those with normal-renin essential hypertension (NREH). Patients with LREH were older and excreted less potassium than patients with NREH or normotensive controls. We conclude that the reduced PG excretion immediately after furosemide administration in patients with EH reflects a diminished capacity of the hypertensive kidney to generate prostaglandins which exert an overall vasodilating effect. Since renin secretion is under the control of renal PG formation, the decreased responsiveness of plasma renin activity (PRA) observed in patients with EH and predominantly in those with LREH may be the consequence of a decreased renal cortical PG generation. Alternatively, mechanisms that reduce both PRA and PG generation have to be considered.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01721777
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  • 8
    Electronic Resource
    Electronic Resource
    Beziehung zwischen Stoffwechselvorgängen und renalem Ausscheidungsmodus bei Sulfonamiden (1962)
    Springer
    Journal of molecular medicine 40 (1962), S. 32-34 
    Details
    ISSN: 1432-1440
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01483447
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  • 9
    Electronic Resource
    Electronic Resource
    Mineralocorticoid and prolactin response to the dopamine antagonist metoclopramide in patients with primary aldosteronism
    Amsterdam : Elsevier
    Journal of Steroid Biochemistry 19 (1983), S. 1671-1676 
    Details
    ISSN: 0022-4731
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0022-4731(83)90389-8
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  • 10
    Electronic Resource
    Electronic Resource
    Paper chromatographic systems for the separation of aldosterone, 18-hydroxycorticosterone, 18-hydroxydeoxycorticosterone, corticosterone and deoxycorticosterone
    Amsterdam : Elsevier
    Journal of Chromatography A 198 (1980), S. 70-75 
    Details
    ISSN: 0021-9673
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/S0021-9673(00)81198-X
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