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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 56 (1978), S. 23-29 
    ISSN: 1432-1440
    Keywords: Renale Hypertonie ; Entfernung einer Nierenarterienstenose ; Renaler Salz- und Flüssigkeitsverlust ; Renin-Angiotensin System ; Renal hypertension ; Removal of one artery stenosis ; Salt and fluid loss ; Renin-angiotensin system
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The effect of removal of one renal artery stenosis on renal sodium and fluid excretion and on the activity of the renin-angiotensin system (RAS) has been investigated in three types of renal hypertension of rats. Blood pressure fell in all experimental models after declamping, independently of changes in urinary sodium and water excretion or plasma angiotensin II (ANG II). Plasma concentrations of ANG II did not rise in response to salt and fluid loss induced by declamping when the contralateral kidney had been removed or when it was depleted from renin. A high renin content of the declamped kidney prevented major salt and fluid loss, whereas renin depletion of this kidney was accompanied by an exaggerated natriuresis and diuresis. Besides this tubular modulation of renal salt and water handling by the local RAS, glomerular filtration rate could be reduced by a stimulated activity of this system in plasma, indicated by a close relationship between serum urea and plasma ANG II levels.
    Notes: Zusammenfassung An drei verschiedenen Modellen des renalen Hochdrucks der Ratte wurde der Einfluß der Entfernung einer Nierenarterienstenose auf die renale Salz- und Wasserausscheidung, die Aktivität des Renin-Angiotensin Systems und die Höhe des Blutdrucks untersucht. Der erhöhte Blutdruck fiel nach Entklammerung in allen Modellen auf Normalwerte ab, unabhängig von den ausgeschiedenen Mengen an Salz und Flüssigkeit und den Änderungen der Plasma Angiotensin II Konzentrationen. Dabei wurden stimulierte Werte für Angiotensin II im Plasma als Folge des Salz- und Flüssigkeitsverlustes nach Entklammerung nur dann beobachtet, wenn die kontralaterale Niere nicht zuvor bereits entfernt oder reninverarmt war. Der plötzliche Anstieg des renalen Perfusionsdruckes nach Entfernung der Stenose führte zu starken Salz- und Flüssigkeitsverlusten, wenn der Reningehalt der betreffenden Niere gering war, während ein hoher Nierenreningehalt mit einer verringerten Elektrolyt- und Wasserausscheidung einherging. Neben dieser tubulären Modulation der renalen Salz- und Wasserausscheidung durch das lokale Nierenrenin-Angiotensin System kann die Stimulation dieses Systems im Plasma über Veränderungen der glomerulären Filtrationsrate die Nierenfunktion beeinflussen. Dies wird deutlich in Situationen, die mit renalem Salz- und Wasserverlust einhergehen; dabei finden sich enge Beziehungen zwischen der Höhe der Plasma-Harnstoff- und der Angiotensin II Werte.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1440
    Keywords: Angiotensin II ; Diabetes insipidus Ratten ; Antidiurese ; SQ 14 225 ; Furosemid ; Angiotensin II ; Diabetes insipidus rats ; Antidiuresis ; SQ 14225 ; Furosemide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Brattleboro rats homozygous for hypothalamic hereditary diabetes insipidus (DI rats) were used to investigate the following questions: a) Do exogenous and endogenous angiotensin II (AII) have an antidiuretic effect in diabetes insipidus? b) Does AII mediate the antidiuresis induced by furosemide? The following results were obtained: 1. AII (5 mg/kg s.c. in oil) and furosemide (50 mg/kg i.p.) decreased urine flow and increased urinary sodium excretion. Furosemide led to a two-fold increase of AII plasma concentrations and a decrease of plasma sodium levels. 2. SQ 14 225 (2×2.5 mg/kg p.o.), an angiotensin I-converting enzyme inhibitor, led to an increase of urine flow and to a slightly elevated urinary sodium excretion. 3. When the formation of AII was blocked by SQ 14 225 (2×2.5 mg/kg p.o.), AII plasma concentrations were 2.5-fold decreased, but furosemide still reduced urine flow. We conclude that plasma AII might have an antidiuretic action in DI rats. However, AII does not mediate the antidiuresis induced by furosemide.
    Notes: Zusammenfassung Bei Brattleboro-Ratten mit hereditärem hypothalamischen Diabetes insipidus (DI Ratten) wurden folgende Fragen untersucht: a) Wirken exogenes and endogenes Angiotensin II (AII) antidiuretisch bei Diabetes insipidus? b) Vermittelt AII den antidiuretischen Effekt von Furosemid? Ergebnisse: 1. AII (5 mg/kg s.c. in Ö1) und Furosemid (50 mg/kg i.p.) verminderten die Urin- und erhöhten die renale Natriumausscheidung. Furosemid führte zu einem zweifachen Anstieg der AII Plasma Konzentration und zur Verminderung der Plasma-Natrium Konzentration. 2. SQ 14 225 (2×2,5 mg/kg p.o.), ein Hemmer des Angiotensin I Converting Enzym, führte zu einer Zunahme der Urin- und der renalen Natriumausscheidung. 3. Auch wenn die Bildung von AII mit SQ 14 225 (2×2,5 mg/kg p.o.) blockiert wurde, reduzierte Furosemid die Urinausscheidung, obwohl die AII Plasma Konzentration 2,5fach vermindert war. Wir schließen daraus, daß Plasma AII bei DI Ratten antidiuretisch wirken kann. Allerdings vermittelt AII nicht den antidiuretischen Effekt von Furosemid.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 56 (1978), S. 87-90 
    ISSN: 1432-1440
    Keywords: β-Rezeptorenblocker ; peripherer Widerstand ; β 1-Selektivität ; β-adrenergic blocking agents ; Peripheral resistance ; β 1-selectivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary The effects of the beta-adrenergic blocking agents propranolol, pindolol, atenolol, bunitrolol, and methypranol on the vascular resistance of isolated perfused hindlimbs of rats were investigated. At concentrations of 0.01 µg/ml in the perfusate dl-propranolol und pindolol significantly increased vascular resistance by blockade ofβ 2-receptor mediated vasodilatation, whereas atenolol, bunitrolol and methypranol had no effect on peripheral resistance at this concentration. With increasing concentrations up to 10 µg/ml all drugs, with the exception of atenolol, caused vasodilatation. We conclude that the specificity of beta-blocking agents can be established in the isolated perfused hindlimb vasculature of rats through its effect on vascular resistance. The lack of inhibition of vascularβ 2-receptors at low concentrations of atenolol and also bunitrolol and methypranol show relative selectivity forβ 1-receptors. The differential effects ofβ-adrenergic agents on vascular resistance may have significance for the clinical use of the drugs.
    Notes: Zusammenfassung Untersucht wurde der Einfluß derβ-Rezeptorenblocker Propranolol, Pindolol, Atenolol, Bunitrolol und Methypranol auf den Gefäßwiderstand der isoliert perfundierten Hinterextremität der Ratte. Bei einer Konzentration von 0,01 µg/ml im Perfusat erhöhten dl-Propranolol und Pindolol den Widerstand deutlich, da die durchβ 2-Rezeptoren vermittelte Vasodilatation ausgeschaltet wurde. Atenolol, Bunitrolol und Methypranol hatten dagegen bei dieser Konzentration keinen Einfluß auf den peripheren Widerstand. Mit steigenden Konzentrationen bis zu 10 µg/ml wirkten alle Pharmaka mit Ausnahme von Atenolol vasodilatatorisch. Wir folgern, daß die Selektivität derβ-Rezeptorenblocker in der isoliert perfundierten Hinterextremität der Ratte durch ihren Effekt auf den Gefäßwiderstand festgestellt werden kann. Wie Atenolol zeigen auch Bunitrolol und Methypranol relative Selektivität fürβ 1-Rezeptoren, da sie in niedrigen Konzentrationen die vaskulärenβ 2-Rezeptoren nicht beeinflussen. Der unterschiedliche Einfluß derβ-Rezeptorenblocker auf den Gefäßwiderstand könnte für die klinische Anwendung der Medikamente Bedeutung haben.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 63 (1985), S. 989-999 
    ISSN: 1432-1440
    Keywords: Dehydration ; Hemodynamics ; Hypertension ; Vasopressin ; Vasopressin antagonists
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The two major biological actions of vasopressin are antidiuresis and vasoconstriction. The antidiuretic action of low concentrations of vasopressin is well established and concentrations 10 to 100 times above those required for antidiuresis elevate arterial blood pressure. Antidiuresis is mediated by V2-receptors at the kidney, whereas vasopressin constricts arterioles by binding at V1-receptors. Pharmacological effects of specific antagonists of the vasoconstrictor activity of vasopressin (vascular or V1-receptor antagonists) are presented. Low concentrations of vasopressin do have significant hemodynamic effects. Physiological concentrations of vasopressin cause vasoconstriction and elevate systemic vascular resistance. In subjects with intact cardiovascular reflex activity, however, cardiac output falls concomitantly and blood pressure therefore does not change. In animals with baroreceptor deafferentation or in patients with blunted baroreceptor reflexes (autonomic insufficiency) a rise in plasma vasopressin causes vasoconstriction and an increase in blood pressure, because cardiac output does not fall under these conditions. Vasopressin contributes substantially via increase in systemic vascular resistance to maintain blood pressure during water deprivation. During hemorrhage and hypotension vasopressin has a major role to restore blood pressure. In experimental hypertension vasopressin contributes to the development and maintenance of high blood pressure in DOCA, but not in genetic hypertensive rats. The role of vasopressin in human hypertension is not yet clear. Vasopressin in extrahypothalamic areas of the brain affects circulatory regulation by interaction with central cardiovascular control centers. The exact mechanism of how vasopressin is involved in central regulation of blood pressure remains to be established. In contrast to our previous opinion vasopressin is a vasoactive hormone also at low plasma concentrations. Its cardiovascular action is more complex than previously assumed.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Springer
    Journal of molecular medicine 56 (1978), S. 131-138 
    ISSN: 1432-1440
    Keywords: Sympathische Aktivität ; Plasma Noradrenalin ; Adrenalin ; Dopamin ; Gefäßreaktivität ; Uptake Aktivität ; Genetische Hypertonie ; Sympathetic activity ; Plasma noradrenaline ; Adrenaline ; Dopamine ; Vascular reactivity ; Uptake activity ; Spontaneous hypertension
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Differences in sympathetic vascular tone between Wistar Kyoto rats (WKR) and stroke prone spontaneously hypertensive rats (spSHR) were determined by comparing the following parameters: sympathetic activity was evaluated by determinations of plasma catecholamines (noradrenaline, adrenaline, dopamine) combined with the measurement of the neuronal and extraneuronal uptake of noradrenaline using an isolated rat heart preparation. The responsiveness of vascular smooth muscle to vasopressor agents was tested in the isolated perfused hindlimb preparation. At the age of 5, 12, 15, and 28 weeks sympathetic nervous activity was significantly higher in spSHR than in WKR since plasma noradrenaline was elevated by almost 50% in the presence of an unaltered activity of the uptake mechanisms. The responsiveness of vascular smooth muscle to noradrenaline was markedly enhanced in spSHR. Besides increased maximal vasoconstriction in response to BaCl2 (20 mmol/l) after potassium chloride depolarization or supramaximal doses of noradrenaline (10−3 mol/l), a supersensitivity of vascular smooth muscle to noradrenaline could also be detected in spSHR (age 5 weeks). The threshold dose and the ED50 were reduced by 25% in spSHR in response to noradrenaline infusions. No changes in threshold or ED50 were found in response to potassium chloride depolarization. The stimulated sympathetic activity in spSHR and the increased responsiveness of resistance vessels to noradrenaline, both contribute to the rise in sympathetic vascular tone. The finding of an increased sympathetic vascular tone in very early stages of hypertension suggest that this factor, producing a primary increase in total peripheral resistance underlies the development of high blood pressure in spSHR.
    Notes: Zusammenfassung Unterschiede des sympathischen Gefäßtonus zwischen spontan hypertonen Ratten (spSHR) und Wistar Kyoto Ratten (WKR) wurden an Hand folgender Größen erfaßt: Die sympathische Aktivität wurde ermittelt durch die Bestimmung der Plasmakatecholamine (Noradrenalin, Adrenalin und Dopamin) bei gleichzeitiger Messung der neuronalen und extraneuronalen Wiederaufnahme von Noradrenalin im isolierten Präparat (Langendorff Herz). Die Ansprechbarkeit glatter Gefäßmuskulatur auf vasopressorische Substanzen wurde in der isoliert perfundierten Hinterextremität der Ratte gemessen. Die sympathische Aktivität war bei spSHR im Alter von 5, 12, 15 und 28 Wochen gesteigert, da die Konzentration von Noradrenalin im Plasma um 50% bei unveränderter neuronaler und extraneuronaler Wiederaufnahme erhöht war. Die Ansprechbarkeit der glatten Gefäßmuskulatur gegenüber Noradrenalin war bei spSHR verstärkt. Neben einer stärkeren maximalen Vasokonstriktion nach supramaximalen Dosen von Noradrenalin (10−3 mol/l) oder BaCl2 (20 mmol/l) fand sich eine spezifische Überempfindlichkeit der einzelnen glatten Muskelzelle gegenüber Noradrenalin bei 5 Wochen alten spontan hypertonen Ratten. Während nach Kaliumdepolarisation keine Unterschiede in der Schwellendosis oder der ED50 auftraten, waren diese bei spSHR für die Noradrenalin-induzierten Widerstandserhöhungen um 25% vermindert. Die stimulierte sympathische Aktivität sowie die erhöhte Ansprechbarkeit der Widerstandsgefäße gegenüber Noradrenalin bei spSHR sind Ursache des gesteigerten sympathischen Gefäßtonus, der über eine Erhöhung des peripheren Widerstandes die Entwicklung des hohen Blutdrucks bei der genetischen Hypertonie der Ratte verursacht.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 152 (1993), S. 301-305 
    ISSN: 1432-1076
    Keywords: Hyponatraemia ; Syndrome of inappropriate antidiuretic hormone secretion ; Vasopressin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Hyponatraemia is one of the most common electrolyte abnormalities in hospitalised children. In a prospective study we tested whether hyponatraemia is associated with sustained release of the antidiuretic hormone arginine vasopressin (AVP). Out of 27 children with persistent hyponatremia (serum sodium 〈130 mmol/l), 25 had measurable plasma concentrations of AVP [median and quartiles 5.0 pg/ml (1.5–8.3)]. Volume contraction as consequence of sodium loss caused hyponatraemia in 16 patients. Hyponatraemia in the presence of extracellular volume expansion and reduced effective arterial blood volume occurred in 5 patients. Only 3 patients had normovolaemic hyponatraemia (so-called syndrome of inappropriate antidiuretic hormone secretion) and 3 suffered from chronic renal failure. It is concluded that plasma AVP concentration is measurable in most children with hyponatraemia. Non-osmotic stimulation of AVP release and lack of suppression of this hormone is an important pathogenetic mechanism of hyponatraemia in children.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 154 (1995), S. 582-584 
    ISSN: 1432-1076
    Keywords: Pyelonephritis ; Hyponatraemia ; Hyperkalaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Abstract Three children with severe hyponatraemia and hyperkalaemia associated with acute pyelonephritis are reported. All were very young male infants in a poor general condition and seriously dehydrated. Diagnostic procedures did not detect obstructive uropathy or vesico-ureteric reflux. Conclusion Hyponatraemia and hyperkalaemia occurs in young infants with severe acute pyelonephritis in the absence of obstructive uropathy or vesico-ureteric reflux. The severe inflammation of the kidney itself may explain the electrolyte disturbance by a transient resistance of the distal tubule to aldosterone.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 152 (1993), S. 59-63 
    ISSN: 1432-1076
    Keywords: Hypertension, renal ; Central nervous system ; Convulsions ; Hypertensive encephalopathy ; Intracranial haemorrhage
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Involvement of the central nervous system (CNS) is a major complication of renal hypertension and is usually due to hypertensive encehalopathy. During a 17-year period we observed 25 children with renal hypertension associated with CNS manifestations in the absence of (group A) and 33 in the presence of advanced renal failure (group B). Convulsions were the most important symptom (65% in both groups combined). Other manifestations were reduced consciousness (69%), visual disturbances (28%), hemiplegia (14%), and cranial nerve palsy (10%). In 56% of children in group A, hypertension was recognised only after appearance of CNS symptoms. Three patients in group A and 19 in group B died. Intracranial haemorrhage associated with hemiplegia was found in 3 cases. From 1970–1977 to 1978–1986 the number of patients and the mortality in group B declined dramatically, probably as a result of improved antihypertensive and renal replacement therapy. In contrast, in group A the number of patients and of CNS symptoms remained similar. The study underlines the importance of frequent blood pressure monitoring in presence of acute or chronic renal disease.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    European journal of pediatrics 154 (1995), S. 582-584 
    ISSN: 1432-1076
    Keywords: Key words Pyelonephritis ; Hyponatraemia ; Hyperkalaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Three children with severe hyponatraemia and hyperkalaemia associated with acute pyelonephritis are reported. All were very young male infants in a poor general condition and seriously dehydrated. Diagnostic procedures did not detect obstructive uropathy or vesico-ureteric reflux. Conclusion Hyponatraemia and hyperkalaemia occurs in young infants with severe acute pyelone-phritis in the absence of obstructive uropathy or vesico-ureteric reflux. The severe inflammation of the kidney itself may explain the electrolyte disturbance by a transient resistance of the distal tubule to aldosterone.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1076
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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