Cardiology pp 297-307 | Cite as

Pathogenetic Mechanisms in Essential Hypertension

  • Franz H. Messerli
  • Edward D. Frohlich


Major parts of the etiology and pathogenesis of hypertension remain fragmentary and hypothetical. Over the past few years,1–5 investigative attention has focused more and more on the hypothesis of Dah16 that a circulating natriuretic substance might be the culprit of the increase in arterial pressure. This concept proposes that a genetic defect of sodium metabolism causing a discrete positive sodium balance might stimulate secretion of a naturiuretic hormone. Thus, normal sodium balance in the prehypertensive patient could be achieved by continuous high levels of naturiuretic hormone. However, sodium transport inhibition would occur not only along the nephron but in other tissues as wel1.4,7,8 In vascular smooth muscle it would increase the reactivity and tone of arteriolar and venous smooth muscle, thereby elevating arterial pressure and diminishing the venous compliance. Constriction of capacitance vessels would, in turn, shift the total blood volume from the periphery toward the cardiopulmonary area. This expansion of cardiopulmonary volume would further perpetuate the secretion of the sodium transport inhibitor from the hypothalamus (even in the presence of a normal or contracted total blood volume) and a vicious circle would ensue.


Cardiac Output Essential Hypertension Total Peripheral Resistance Total Blood Volume Borderline Hypertension 
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Copyright information

© Springer Science+Business Media New York 1984

Authors and Affiliations

  • Franz H. Messerli
    • 1
  • Edward D. Frohlich
    • 1
  1. 1.Department of Internal Medicine Section on Hypertensive DiseasesOchsner Medical InstitutionsNew OrleansUSA

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