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  • 1
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 116 (1994), S. 2717-2724 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    s.l. : American Chemical Society
    Journal of the American Chemical Society 114 (1992), S. 3197-3200 
    ISSN: 1520-5126
    Source: ACS Legacy Archives
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In vitro andex vivo effects of propranolol on platelet aggregation, formation of thromboxane B2 (TXB2) and platelet sensitivity to prostacyclin were studied in healthy men. Propranolol, addedin vitro to platelet rich plasma (PRP) inhibited platelet aggregation and TXB2 formation induced by ADP, 1-epinephrine, collagen and arachidonic acid. Concentration of 20–100 μM propranolol were effective when ADP, 1-epinephrine and collagen were used as stimuli. Higher concentrations (250–500 μM) were needed to inhibit aggregation induced by arachidonic acid. Oral administration of propranolol either as a single dose (120 mg) or for one week (3×40 mg/day) did, however, not affect platelet aggregation, thromboxane formation and platelet sensitivity to prostacyclin. In addition, withdrawal of propranolol was without effect on these parameters. Although propranolol has potent effects on platelet functionin vitro, it seems that the blood levels achievable by oral administration of propranolol are too low to affect platelet aggregation and TXB2 formation.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 53 (1975), S. 177-180 
    ISSN: 1432-1440
    Keywords: AVP release ; angiotensin ; ADH-Freisetzung ; Angiotensin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung In vitro wird die Freisetzung von ADH aus der Neurohypophyse der Ratte durch Zugabe von Angiotensin (AII) signifikant gesteigert; entsprechend ist am Hund in vivo eine Stimulation der ADH-Abgabe nach AII nachweisbar. Beides läßt auf eine enge Beziehung des Renin-Angiotensin-Aldosteron-Systems mit ADH schließen. Um auch beim Menschen nähere Aussagen hierüber zu gewinnen, wurde ein sensitiver Radioimmunoassay für ADH entwickelt [17, 18]. Die gemessenen basalen ADH-Werte entsprechen den in der Literatur mitgeteilten Daten und betragen 3,4±2,2 pg/ml. Nach AII-Infusion (3–30 ng/min·kg) kommt es zu einem signifikanten Anstieg auf das 2–5fache des Ausgangswertes. Innerhalb von 90 min kehren die Werte wieder auf den Ausgangsbetrag zurück. Zur Kontrolle eines wirksamen AII-Spiegels diente die Erhöhung des Blutdruckes um ca. 20 mm Hg. Der Plasmareninwert nahm innerhalb dieser Zeit ab, Osmolalität und Elektrolytkonzentration des Plasmas änderten sich nicht. Eine Freisetzung von ADH durch die Erhöhung des Blutdruckes per se scheint äußerst unwahrscheinlich zu sein, da bei der zu gleichem Druckanstieg führenden Gabe von Noradrenalin keine Erhöhung des ADH-Spiegels im Plasma gefunden wurde.
    Notes: Summary Release of arginine vasopressin (AVP) from rat neurohypophysis in in vitro studies is significantly augmented by the addition of angiotensin (AII), and in in vivo studies in dogs renin and AII were found to stimulate secretion of AVP. Both these results suggest the existence of a direct relationship between the salt regulating renin-angiotensin-aldosterone system and the water controlling AVP system. To evaluate whether such observations apply also in man a sensitive double antibody radioimmunoassay for AVP was developed [17, 18]. Basal plasma levels of AVP in recumbent humans without salt and fluid restriction at room temperature were 3.4±2.2 pg/ml, and 30 min after the onset of an AII infusion at a concentration of 3–30ng/min·kg, a significant increase of AVP was found. Maximum measurements were 2–5 times basal levels which returned to normal within 90 min. During the AII infusion one also noted a 20 mm Hg rise in blood pressure, accompanied by a significant decrease in plasma renin activity. During the same period serum osmolality and serum sodium concentration did not change. Elevation of blood pressure by norepinephrine was not followed by any detectable change of plasma AVP levels, thus excluding a nonspecific blood pressure effect.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 58 (1980), S. 1099-1104 
    ISSN: 1432-1440
    Keywords: Juvenile Hypertonie ; Niere ; Prostaglandine ; Kallikrein ; Renin ; Juvenile hypertension ; Kidney ; Prostaglandins ; Kallikrein ; Renin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Essential hypertension in infancy, once believed to occur rarely if ever, is now increasingly recognized as a potential precursor of essential hypertension in adulthood. The mechanisms responsible for hypertension in childhood and adolescence are only beginning to be delineated. Renal factors assumed to be operative in juvenile hypertension are involving either volume control (by renal regulation of sodium-chloride and water balance) or vasoactive substances like the kallikrein-kinin, the renin-angiotensin and the prostaglandin system and other less well defined hormones. There is a close interrelationship of all these hormones with each other as well as a close linking of these vasoactive compounds to the renal regulation of sodium-chloride and water balance, thus interfering with a major environmental factor necessary for the development of essential hypertension. At present, data are insufficient to delineate a single hormone or a single hemodynamic abnormality as the only primary factor in juvenile hypertension. Further research into the pathomechanisms responsible for the elevation of blood pressure at its very beginning will improve our understanding of hypertension and possibly benefit its management by early intervention.
    Notes: Zusammenfassung Abweichend von früheren Auffassungen wird heute zunehmend die essentielle Hypertonie als eine Erkrankung auch des Kindes- und Jugendalters angesehen, aus der sich später die essentielle Hypertonie des Erwachsenen entwickelt. Die zur Entstehung der juvenilen Hypertonie führenden Pathomechanismen wurden in klinischen, epidemiologischen und tierexperimentellen Studien untersucht. Zu den renalen Mechanismen, die wahrscheinlich bei der Entstehung der juvenilen Hypertonie eine Rolle spielen, gehören Faktoren, die die renale Kontrolle der Salz-Wasser-Bilanz beeinflussen und vasoaktive Substanzen wie das renale Kallikrein-Kinin-System, das Renin-Angiotensin-System, das Prostaglandin-System und andere bislang weniger gut definierte Hormone. Diese renalen Hormone haben zahlreiche Wechselwirkungen untereinander. Neben ihren direkten Wirkungen auf die Gefäßwand können sie die Salz-Wasser-Bilanz beeinflussen bzw. werden von ihr beeinflußt, wodurch eine enge Verbindung mit Kochsalz, dem wohl entscheidendsten Umweltfaktor für die Entstehung der essentiellen Hypertonie, hergestellt ist. Fortgesetzte Bemühungen um die Aufklärung insbesondere der renalen Pathomechanismen, die am Beginn der Blutdruckerhöhung im Kindes- und Jugendalter wirksam sind, werden das Verständnis der essentiellen Hypertonie verbessern und unter Umständen durch frühzeitige Intervention sogar die Prävention dieser Erkrankung ermöglichen.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 60 (1982), S. 479-488 
    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
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  • 7
    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
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  • 8
    ISSN: 1432-1440
    Keywords: Pheochromocytoma ; MIBG scintigraphy ; Intraoperative staging
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Metaiodobenzylguanidine (MIBG) imaging is a well-established method for locating intra-and extraadrenal pheochromocytomas. We investigated whether preoperative injection of 123-I-MIBG might be useful for intraoperative staging of chromaffine tumor cells. This was performed in a 46-year-old patient in whom the diagnosis of a malignant pheochromocytoma had been established by 123-I-MIBG imaging and enhanced catecholamine secretion. The rationale for intraoperative staging in this patient was a discrepancy between computed tomography (CI) of the abdomen and the radionuclide imaging, because scintigraphy revealed a mass with MIBG uptake in the right lower abdomen that could not be visualized by CT. We thus applied a preoperative dose of 4 mCi 123-I-MIBG and determined tissue activity by direct organ measurement. A right abdominal mass was thus identified with an activity of 10×104 impulses/s as compared to normal tissue (15×102). The left-sided tumor was found to be identified correctly by prior CT and MIBG imaging. We thus conclude that intraoperative application of this single probe measurement might help to identify chromaffine tumor cells that have not been located fully by CT.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-1440
    Keywords: Renal prostaglandins ; Essential hypertension ; Plasma renin activity ; Renale Prostaglandine ; essentielle Hypertonie ; Plasmareninaktivität
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die renale Prostaglandin (PG)-Ausscheidung und die Stimulierbarkeit der Reninsekretion wurde bei Patienten mit essentieller Hypertonie (n=35) und bei altersgleichen normotensiven Kontrollpersonen (n=22) vergleichend untersucht. Bei den Patienten mit essentieller Hypertonie wurde eine erniedrigte basale Ausscheidung des vasodilatierenden PGE2 (p〈0,02) bei im Normbereich liegender Ausscheidung des vasokonstriktorischen PGF2α im Urin festgestellt. Darüber hinaus stieg innerhalb der ersten 15 min nach i.v.-Gabe von 40 mg Furosemid die PGE2-Ausscheidung bei Patienten mit essentieller Hypertonie signifikant geringer an als bei den Kontrollpersonen (p〈0,001), während der Anstieg der PGF2α-Ausscheidung in beiden Gruppen gleich war. Zum gleichen Zeitpunkt lag der prozentuale Anstieg der Plasmareninaktivität nach Furosemid bei Hypertonikern (167±11 (SEM)) deutlich unter dem Anstieg der Kontrollgruppe (386±46,p〈0,001). Unsere Ergebnisse unterstützen die Annahme, daß eine erniedrigte renal-kortikale, (vaskuläre?) Synthese vasodilatierender Prostaglandine die Ursache sowohl für die verminderte Stimulierbarkeit der Reninsekretion als auch für den gesteigerten renalen Gefäßwiderstand bei essentieller Hypertonie ist.
    Notes: Summary Under basal conditions prostaglandin (PG) E2-excretion was significantly lower in 35 patients with essential hypertension studied than in 22 age-and sex-matched controls (p〈0.02). PGF2α-excretion was similar in both groups. Within the first 15 minutes after furosemide i.v., PGE2-excretion rose substantially less in the patients than in the controls (p〈0.001), while the increase in PGF2α-excretion was not different for both groups. The coincident rise of plasma renin activity was significantly lower in the hypertensive (167%±11, SEM) than in the normotensive (386%±46) group (p〈0.001). Our results support the assumption that a decrease in renal cortical (vascular?) synthesis of vasodilatating PG's may be the cause for both, the diminished secretion of renin and the increase of vascular resistance in the kidney, which are often associated in essential hypertension.
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 61 (1983), S. 35-42 
    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.
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