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Circulating Natriuretic Factor in the Pathogenesis of Genetic Hypertension of Renal Origin

  • P. Ferrari
  • H. E. de Wardener
  • J. A. Millet
  • L. Torielli
  • M. Ferrandi
  • G. Bianchi
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  • 12 Downloads
Part of the Developments in Nephrology book series (DINE, volume 18)

Abstract

A circulating natriuretic factor, able to inhibit the cellular Na+-K+ pump, has been described in human essential and animal sperimental hypertension (1,2). Increases of this circulating factor seem to be linked to a kidney defect in sodium and water excretion. The Milan hypertensive strain of rats (MHS) spontaneously develops hypertension due to a genetically determined, renal abnormality which produces a transient Na retention during the prehypertensive phase (3). To verify whether a circulating natriuretic factor could be involved in the pathogenesis of MHS hypertension, we have measured in MHS and their normotensive controls (MNS) at different ages the Na transport through the Na+-K+ pump in red blood cells (RBC), and the ability of rat plasma to stimulate “in vitro” the glucose 6-phosphate-dehydrogenase (G6PD) as index of the plasma capacity to inhibit the Na+-K+ ATPase activity(4).

Keywords

Water Excretion Mean Blood Pressure Renal Abnormality Normotensive Control Genetic Hypertension 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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    Ferrari P. et al.: Clin. Sci. 63: 61, 1982Google Scholar
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    Persson E. et al.: Acta Physiol. Scand. 122: 217, 1984PubMedCrossRefGoogle Scholar

Copyright information

© Martinus Nijhoff Publishing, Boston 1987

Authors and Affiliations

  • P. Ferrari
    • 1
  • H. E. de Wardener
    • 2
  • J. A. Millet
    • 2
  • L. Torielli
    • 1
  • M. Ferrandi
    • 1
  • G. Bianchi
    • 3
  1. 1.Farmitalia Carlo Erba Centro RicercheNervianoItaly
  2. 2.Research Laboratories Charing CrossLondonUK
  3. 3.Istituto Scienze MedicheUniversità di MilanoItaly

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