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Enhanced L-arginine-induced vasoreactivity suggests endothelial dysfunction in CADASIL

Nils Peters1, Tobias Freilinger, Christian Opherk

  • 1Dept. of Neurology, Klinikum Grosshadern, Ludwig-Maximilians-University, Marchioninistrasse 15, 81377, Munich, Germany. Nils.Peters@med.uni-muenchen.de

Journal of Neurology
|June 10, 2008
PubMed

Insights

Cerebral artery function is impaired in Cerebral Autosomal-Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL). Enhanced L-arginine vasoreactivity suggests potential therapeutic strategies for CADASIL and small vessel diseases.

Area of Science:

  • Neurology
  • Vascular Biology
  • Genetics

Background:

  • Cerebral Autosomal-Dominant Arteriopathy with Subcortical Infarcts and Leukoencephalopathy (CADASIL) is caused by Notch3 gene mutations, leading to stroke and dementia.
  • Pathological hallmarks include arterial granular deposits and smooth muscle cell degeneration.
  • Endothelial function in CADASIL remains poorly understood, despite its importance in cerebrovascular health.

Purpose of the Study:

  • To assess endothelial function in CADASIL patients by measuring L-arginine-induced vasoreactivity.
  • To compare cerebral hemodynamic parameters between CADASIL patients and healthy controls.

Main Methods:

  • Transcranial Doppler sonography was used to measure middle cerebral artery blood flow velocity and pulsatility index.
  • L-arginine, a substrate for nitric oxide synthase, was administered to assess endothelial-dependent vasoreactivity.
  • 25 CADASIL patients and 24 non-CADASIL controls were included.

Main Results:

  • CADASIL patients showed reduced resting mean flow velocity and increased pulsatility index compared to controls.
  • L-arginine administration significantly increased vasoreactivity in CADASIL patients compared to controls.
  • A significant reduction in pulsatility index was observed after L-arginine in CADASIL patients, indicating improved vasodilation.

Conclusions:

  • Impaired cerebral hemodynamics and endothelial dysfunction likely play a pathogenic role in CADASIL.
  • The enhanced L-arginine vasoreactivity in CADASIL suggests potential therapeutic targets.
  • Findings may offer insights into treating sporadic small vessel diseases as well.
Abstract

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