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Related Experiment Videos

Venodilation in Raynaud's disease

G Bedarida1, D Kim, T F Blaschke

  • 1Division of Clinical Pharmacology, Stanford University Medical Center, CA 94305-5113.

Lancet (London, England)
|December 11, 1993
PubMed
Summary
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Raynaud's disease impairs blood vessel dilation, particularly endothelium-dependent vasodilation. This study suggests impaired nitric oxide release contributes to this vasospastic disorder.

Area of Science:

  • Vascular Biology
  • Cardiovascular Physiology
  • Medical Research

Background:

  • Raynaud's disease is a vasospastic disorder with unclear pathogenesis.
  • Enhanced response to catecholamines is a suspected contributor.
  • Impaired endothelium-dependent dilation is observed in other vasospastic conditions.

Purpose of the Study:

  • To investigate endothelium-dependent and independent venodilatory function in Raynaud's disease.
  • To compare venodilatory responses to noradrenaline and bradykinin between Raynaud's patients and controls.
  • To explore the role of nitric oxide in Raynaud's disease pathogenesis.

Main Methods:

  • Hand-vein compliance technique used to assess venodilatory function.
  • Dose-response curves constructed for noradrenaline (endothelium-independent) and bradykinin (endothelium-dependent).

Related Experiment Videos

  • Nitroprusside used to assess direct nitric oxide-mediated dilation.

    • Main Results:

    • No significant difference in noradrenaline response between Raynaud's and control groups.
    • Significantly lower maximal dilation (Emax) to bradykinin in Raynaud's disease patients (p=0.02).
    • Normal maximal dilation to nitroprusside in Raynaud's patients, indicating intact nitric oxide-mediated vasodilation.

    Conclusions:

    • Endothelium-dependent venodilation is impaired in peripheral vessels in Raynaud's disease.
    • Diminished nitric oxide release may underlie this impairment.
    • Impaired vasodilation likely contributes to the pathogenesis of Raynaud's disease.