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  • 2000-2004  (1)
  • 1985-1989  (2)
  • Hypertension  (2)
  • Critical care  (1)
  • 1
    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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  • 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)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Recovery from withdrawal of inhaled nitric oxide and kinetics of nitric oxide-induced inhibition of nitric oxide synthase activity in vitro (2000)
    Springer
    Intensive care medicine 26 (2000), S. 330-335 
    Details
    ISSN: 1432-1238
    Keywords: Key words Intensive care ; Critical care ; Acute respiratory distress syndrome ; Persistent pulmonary hypertension of the newborn ; Feedback inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To examine the kinetics of successful nitric oxide (NO) withdrawal in vivo and in vitro.¶Design and setting: Prospective study in a university pediatric intensive care ward and research laboratory.¶Patients and materials: Nineteen patients with acute respiratory distress syndrome (ARDS) or persistent pulmonary hypertension of the newborn (PPHN). Primary porcine pulmonary artery cells in vitro.¶Interventions: NO inhalation and withdrawal in patients; exposure to NO donor sodium nitroprusside (SNP) and gaseous NO in vitro.¶Measurements and results: In patients: a slight, but significant, increase of oxygenation index (OI) from 4.57 ± 0.24 cmH2O/torr (mean ± SEM) to 4.90 ± 0.26 cmH2O/torr after withdrawal of NO (p 〈 0.001). Recovery of OI (4.43 ± 0.23 cmH2O/torr) 30 min after weaning, a significant drop after 4 h (3.72 ± 0.17 cmH2O/torr; p 〈 0.001), values restored after 12 h.¶In vitro: NO synthase (NOS) activity was significantly lower in SNP-incubated cells (20.0 ± 4.0 μm/min) than in control cells (37.6 ± 7.0 μm/min; p 〈 0.05). Thirty minutes after SNP withdrawal there was NOS activity of 35.8 ± 10.0 μm/min with a significant increase by 4 h (p 〈 0.05). No alteration of endothelial NOS (ENOS) mRNA expression by NO (Northern Blot).¶Conclusion: In patients there is a slight, but significant, reversible increase of OI after successful weaning from NO. In vitro, NO leads to a reversible decrease of ENOS activity on a post mRNA level, resembling clinical observations.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001340051158
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    Paper (German National Licenses)
    Fulltext
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