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  • Hyperkalaemia  (3)
  • Hyponatraemia  (3)
  • 6-Hydroxydopamine  (1)
  • Angiotensin II  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 313 (1980), S. 155-157 
    ISSN: 1432-1912
    Keywords: Spontaneosly hypertensive rats ; Urinary kallikrein ; Sympathetic activity ; 6-Hydroxydopamine
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Urinary kallikrein excretion was studied in young, stroke-prone, spontaneously hypertensive rats (spSHR). Seven-week-old spSHR were found to excrete more kallikrein into the urine than normotensive Wistar Kyoto control rats (WKR). “Chemical sympathectomy”, induced by 6-hydroxydopamine (6-OHDA) immediately after birth, resulted in normotensive blood-pressure levels and in a reduction of kallikrein in spSHR. In normotensive WKR, blood pressure and urinary kallikrein excretion were only slightly diminished by 6-OHDA. The results suggest a relationship between sympathetic activity and kallikrein excretion, being especially pronounced in spSHR, which have an elevated sympathetic activity.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-198X
    Keywords: Tubular function ; Atrial natriuretic peptide ; Hypertension ; Acidosis ; Hyperkalaemia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A 14-year-old boy with the syndrome of hypertension and hyperkalaemia with normal glomerular filtration rate (Gordon's syndrome) is described. The patient's clinical symptoms consisted of periodic paralysis, slight metabolic acidosis of the proximal type and hypercalciuria. Prostaglandin excretion was normal. Infusion of atrial natriuretic peptide had no effect on electrolyte excretion or glomerular function although a normal increase in cyclic guanosine monophosphate was demonstrated in plasma and urine. This lack of sensitivity to atrial natriuretic peptide offers a new pathophysiological concept in this syndrome. Treatment with hydrochlorothiazide was successful in this case.
    Type of Medium: Electronic Resource
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  • 3
    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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  • 4
    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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  • 5
    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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  • 6
    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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