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Endothelial dysfunction in hypertension. A critical evaluation

P A Van Zwieten1

  • 1Department of Pharmacotherapy, Academic Medical Centre, University of Amsterdam, The Netherlands.

Blood Pressure. Supplement
|January 1, 1997
PubMed
Summary
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The link between endothelial dysfunction and hypertension remains uncertain. While some evidence suggests impaired nitric oxide (NO) synthesis contributes to high blood pressure, other studies show intact endothelial function in hypertensive individuals.

Area of Science:

  • Cardiovascular Research
  • Hypertension Studies
  • Endothelial Function Analysis

Background:

  • Endothelial dysfunction, potentially impairing nitric oxide (NO) mediated vasodilation, is hypothesized to cause hypertension.
  • This hypothesis suggests that damage to blood vessel linings leads to increased blood pressure.

Purpose of the Study:

  • To critically evaluate the evidence supporting and refuting a causative link between endothelial dysfunction and hypertension.
  • To explore discrepancies in findings regarding endothelial function in hypertensive subjects.

Main Methods:

  • Review of existing literature on endothelial dysfunction and hypertension.
  • Analysis of studies involving NO-synthase blockade (L-NAME), L-arginine administration in rats, and forearm vascular bed studies in humans.

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  • Comparison of findings in hypertensive patients and animal models versus control groups.

    • Main Results:

    • Evidence supporting the link includes hypertensive effects of NO-synthase blockade and antihypertensive effects of L-arginine in rats.
    • Impaired forearm vasodilation and diminished NO synthesis in hypertensives also support the association.
    • Contradictory findings include intact endothelial function in some isolated vessels and human forearm studies.

    Conclusions:

    • The association between endothelial dysfunction and hypertension is currently uncertain.
    • Discrepancies in research findings necessitate further investigation to clarify the role of endothelial dysfunction in hypertensive disease.