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  • Articles: DFG German National Licenses  (6)
  • Atrial natriuretic peptide  (4)
  • Hypertension  (2)
  • Adverse effects  (1)
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  • Articles: DFG German National Licenses  (6)
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  • 1
    Electronic Resource
    Electronic Resource
    Durstregulation bei terminaler Niereninsuffizienz (1990)
    Springer
    Journal of molecular medicine 68 (1990), S. 1127-1133 
    Details
    ISSN: 1432-1440
    Keywords: Thirst regulation ; Vasopressin ; Renin-angiotensin-system ; Atrial natriuretic peptide ; Endstage renal disease
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary About 30% of hemodialyzed patients are suffering from chronic fluid overload despite advice to restrict the oral fluid intake. To investigate the cause of the abnormal drinking behaviour a clinical study was performed in 51 non-diabetic patients with endstage renal disease exhibiting lower interdialytic weight gain (〈3 kg,n=17) and increased interdialytic weight gain (〉3 kg,n=34). Blood pressure, body weight self-estimated thirst intensity before and after hemodialysis were analyzed. Biochemical and behavioral variables were measured including hormonal factors of water and sodium metabolism. Significant differences of dry weight, creatinine, urea nitrogen and thirst intensity were found between the two groups. Catecholamines, renin, angiotensin II, aldosterone, vasopressin and atrial natriuretic peptide exhibited a similar pattern in both groups. Atrial natriuretic peptide decreased during hemodialysis in both groups, angiotensin II, however, and norepinephrine showed an exaggerated response to ultrafiltration rate in polydipsic patients. These results suggest that changes in serum osmolality during hemodialysis did not contribute to thirst and drinking behaviour. It seems that postdialytic hypovolaemia together with higher plasma-angiotensin II-levels is responsible for increased oral intake of fluid and excessive weight gain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01798063
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Kardiovaskuläre Wirkung des antidiuretischen Hormons Arginin-Vasopressin (1985)
    Springer
    Journal of molecular medicine 63 (1985), S. 989-999 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF01737635
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Reduction of NO-induced methemoglobinemia requires extremely high doses of ascorbic acid in vitro (1998)
    Springer
    Intensive care medicine 24 (1998), S. 612-615 
    Details
    ISSN: 1432-1238
    Keywords: Key words Nitric oxide ; Methemoglobin ; Methemoglobinemia ; Adverse effects ; Ascorbic acid ; Glutathione
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The objective of the present study was to investigate the treatment of nitric oxide (NO)-induced methemoglobinemia by ascorbate and its consequences on red blood cell (RBC) glutathione in vitro. RBC were obtained from five healthy volunteers. The following experiments were carried out: (1) After methemoglobin generation by NO, ascorbate was added (2) RBC were simultaneously exposed to NO and ascorbate (3) Methemoglobin was generated by NO, ascorbate was added and incubation with NO continued. (1) After discontinuation of NO, the mean half life for methemoglobin was reduced from 195 min (controls) to 60 min (10 mM ascorbate) in a dose-dependent manner. (2) Methemoglobin formation after 3 h of NO exposure was 2.7 ± 0.3 % in controls and 1.8 ± 0.1 % with 10 mM ascorbate (p 〈 0.01). (3) Further methemoglobin formation was inhibited only by 10 mM ascorbate (p 〈 0.001). NO incubation did not affect RBC glutathione (86.5 ± 19.6 and 86.5 ± 19.6 mg/l, respectively). Treatment with 10 mM ascorbate significantly decreased glutathione (p 〈 0.002). In vitro, NO-induced methemoglobin formation is significantly decreased only by a high (10 mM) ascorbate concentration. Glutathione, critical for ascorbate activity, is not influenced by NO.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340050623
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Atrial natriuretic peptide and sodium homeostasis in chronic renal failure (1989)
    Springer
    Pediatric nephrology 3 (1989), S. 397-400 
    Details
    ISSN: 1432-198X
    Keywords: Aldosterone ; Atrial natriuretic peptide ; Chronic renal failure ; Dopamine ; Noradrenaline ; Sodium homeostasis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In order to evaluate the possible role of vasoactive hormones in the mechanism of exaggerated sodium loss due to reduced renal mass we measured plasma concentration of atrial natriuretic peptide (ANP), aldosterone, plasma renin activity (PRA), plasma noradrenaline, and dopamine, in 12 children with advanced chronic renal failure (mean CIn17.8-2.6,x± SEM, CPAH93.5±17 ml/min per 1.73 m2, FENa7.0±0.95%). No patient had clinical signs of volume overload. Plasma concentrations of ANP were not significantly different from those of healthy agematched controls (29.2±7.2 vs 23.2±3.1 fmol/ml) and did not correlate with urinary sodium excretion. Plasma concentrations of aldosterone, PRA and noradrenaline, were also within the physiological range, while plasma dopamine levels were elevated (260±36 vs 98±11 pg/ml, 〈0.001). Our data do not support the notion that ANP or the renin-aldosterone axis play a major role in the adaptation of remaining nephrons to maintain long-term sodium balance in normotensive children with chronic renal failure.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00850214
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    The syndrome of hypertension and hyperkalaemia with normal glomerular function (Gordon's syndrome) (1987)
    Springer
    Pediatric nephrology 1 (1987), S. 473-478 
    Details
    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
    URL: http://dx.doi.org/10.1007/BF00849256
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Atrial natriuretic peptide and cyclic 3′5′-guanosine monophosphate as indicators of fluid volume overload in children with chronic renal failure (1992)
    Springer
    Pediatric nephrology 6 (1992), S. 60-64 
    Details
    ISSN: 1432-198X
    Keywords: Atrial natriuretic peptide ; Cyclic 3′5′-guanosine monophosphate ; Chronic renal failure ; Haemodialysis ; Volume overload
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Plasma atrial natriuretic peptide (ANP) and cyclic 3′5′-guanosine monophosphate (cGMP) were investigated as indicators of fluid volume overload in children and adolescents with chronic renal failure. Plasma ANP and cGMP were measured in both paediatric patients with chronic renal failure (n=17, mean serum creatinine 371±242 μmol/l) and those with end-stage renal disease on haemodialysis (n=18). cGMP was higher in children with chronic renal failure than in 45 healthy controls (1.0±0.4 vs 2.1±0.8 nmol/l,P〈0.01), whereas plasma ANP was similar (26.9±9.7 vs 34.0±12.3 pmol/l). Both ANP and cGMP were markedly elevated in children with end-stage renal disease before haemodialysis and fell significantly during dialysis. During dialysis body weight decreased by 1.6±0.7 kg, corresponding to 4.5±2.1% of body weight. Plasma ANP correlated positively with plasma cGMP in haemodialysed patients (r=0.43,P〈0.05). Reduction in body weight and in mean arterial pressure correlated more closely with plasma ANP than with cGMP. Therefore, elevation of plasma ANP appears to indicate volume overload in children undergoing haemodialysis, but whether it can be used also in children with chronic renal failure requires further investigation
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00856837
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    Paper (German National Licenses)
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