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The Relation of a Circulating Sodium Transport Inhibitor to Essential Hypertension

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Kidney in Essential Hypertension

Part of the book series: Developments in Cardiovascular Medicine ((DICM,volume 35))

Abstract

It is postulated that the increase in peripheral resistance in essential hypertension is largely due to the observed rise in the circulating level of a sodium transport inhibitor. Evidence is presented to suggest a link between a genetic abnormality in the kidney’s capacity to excrete sodium, the excessive secretion of a sodium-transport inhibitor, salt intake, the rise in peripheral resistance, and ultimately the development of essential hypertension.

When the volume of body fluids is expanded, the plasma acquires natriuretic properties (1), and its capacity to inhibit sodium transport increases (2). It is not known whether these two phenomena are due to a change in the concentration of the same substance. Some workers (3, 4) claim that one substance is responsible, that it is of small molecular weight (approximately 1000 daltons), that it is present in plasma and urine, that it inhibits Na+-K+-ATPase, cross-reacts against digoxin antibodies, and displaces tritiated ouabain from the surface of red cells. Others, including ourselves, would agree with the first group that there is a substance of small molecular weight present in plasma and urine which inhibits Na+-K+-ATPase (5), but we do not find that it cross-reacts with digoxin antibodies or displaces tritiated ouabain from the surface of red cells (unpublished observation). A third group has obtained a larger substance (probably greater than 5000 daltons) from the left auricle which is natriuretic but does not inhibit Na+-K+-ATPase (6, 7, 8). It is not yet known whether this substance is present in the plasma of the urine. This paper presents the relation to essential hypertension of the substance present in the plasma and urine which inhibits Na+-K+-ATPase but does not otherwise resemble digoxin.

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Authors
  1. H. E. de Wardener
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  2. G. A. MacGregor
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Editor information

Editors and Affiliations

  1. Hemodynamic Laboratory, Ochsner Clinic and Alton Ochsner Medical Foundation, 1514 Jefferson Highway, New Orleans, Louisiana, 70121, USA

    Franz H. Messerli MD (Director Associate Professor of Medicine) (Director Associate Professor of Medicine)

  2. Tulane University School of Medicine, New Orleans, Louisiana, USA

    Franz H. Messerli MD (Director Associate Professor of Medicine) (Director Associate Professor of Medicine)

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© 1984 Martinus Nijhoff Publishing, Boston/The Hague/Dordrecht/Lancaster

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de Wardener, H.E., MacGregor, G.A. (1984). The Relation of a Circulating Sodium Transport Inhibitor to Essential Hypertension. In: Messerli, F.H. (eds) Kidney in Essential Hypertension. Developments in Cardiovascular Medicine, vol 35. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-3897-0_1

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  • DOI: https://doi.org/10.1007/978-1-4613-3897-0_1

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4613-3899-4

  • Online ISBN: 978-1-4613-3897-0

  • eBook Packages: Springer Book Archive

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