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AT1 receptor blockade prevents the decrease in conduit artery flow-mediated dilatation during NOS inhibition in

Jeremy Bellien1, Michele Iacob, Helene Eltchaninoff

  • 1Department of Pharmacology, Institut National de la Santé et de la Recherche Medicale (INSERM) U644, Institut Federatif de Recherche Multidisciplinaire sur les Peptides 23, Rouen University Hospital, Rouen Cedex, France.

Clinical Science (London, England : 1979)
|November 28, 2006
PubMed
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Angiotensin II type 1 receptor blockade prevents flow-mediated dilatation reduction during nitric oxide synthase inhibition in healthy humans. This suggests a compensatory endothelial mechanism, possibly involving endothelium-derived hyperpolarizing factor.

Area of Science:

  • Cardiovascular Physiology
  • Endothelial Function
  • Pharmacology

Background:

  • Flow-mediated dilatation (FMD) assesses endothelial function.
  • Nitric oxide synthase (NOS) inhibition reduces FMD.
  • The role of alternative endothelial pathways during NOS inhibition is unclear.

Purpose of the Study:

  • To investigate if AT(1) receptor blockade prevents FMD decrease during NOS inhibition.
  • To explore compensatory endothelial mechanisms in humans.

Main Methods:

  • Randomized, double-blind, cross-over study in 12 healthy subjects.
  • Measured radial artery FMD using Doppler and echotracking.
  • Administered L-NMMA for NOS inhibition and telmisartan for AT(1) blockade.
  • Assessed prostacyclin and EDHF roles with aspirin and fluconazole.

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Main Results:

  • Telmisartan prevented the L-NMMA-induced decrease in FMD.
  • Baseline parameters and endothelium-independent dilatation were unaffected.
  • The compensatory mechanism appeared independent of prostacyclin.
  • Endothelium-derived hyperpolarizing factor (EDHF) may be involved.

Conclusions:

  • AT(1) receptor blockade preserves FMD during NOS inhibition in humans.
  • A compensatory endothelial pathway likely develops.
  • This pathway may involve EDHF, not prostacyclin.