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Related Experiment Videos

Mechanisms underlying nitrate-induced endothelial dysfunction: insight from experimental and clinical studies.

Ascan Warnholtz1, Nikolaus Tsilimingas, Maria Wendt

  • 1Division of Cardiology, University Hospital Hamburg-Eppendorf, Hamburg, Germany.

Heart Failure Reviews
|October 16, 2002
PubMed
Summary

Nitrate tolerance, caused by nitroglycerin (NTG), involves pseudotolerance and intrinsic vascular changes. Oxidative stress and peroxynitrite formation contribute to tolerance, which can be mitigated by antioxidants and ACE inhibitors.

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Area of Science:

  • Cardiovascular Pharmacology
  • Vascular Biology
  • Biochemistry

Background:

  • Nitroglycerin (NTG) effectiveness is limited by rapid tolerance development.
  • Pseudotolerance mechanisms, including neurohormonal activation and volume expansion, can blunt NTG's vasodilatory effects.
  • Long-term NTG use may alter vascular responsiveness due to intrinsic changes.

Purpose of the Study:

  • To explore mechanisms underlying nitrate tolerance and cross-tolerance.
  • To investigate the role of oxidative stress in NTG-induced endothelial dysfunction.
  • To discuss the impact on the NO/cyclicGMP pathway.

Main Methods:

  • Review of experimental work on nitrate tolerance mechanisms.
  • Identification of enzymes involved in superoxide production (NADPH oxidase, nitric oxide synthase).

Related Experiment Videos

  • Analysis of peroxynitrite formation and its consequences.

    • Main Results:

    • Increased vascular superoxide production and protein kinase C activation contribute to tolerance.
    • Peroxynitrite formation, from NTG-derived radicals and NO, may cause tolerance and cross-tolerance.
    • Antioxidants (e.g., Vitamin C) and oxidative stress reducers (ACE inhibitors, AT1 blockers, folic acid) show beneficial effects.

    Conclusions:

    • Oxidative stress is a key factor in nitrate tolerance and cross-tolerance.
    • Therapies targeting oxidative stress may improve NTG efficacy and endothelial function.
    • Further research will focus on oxidative stress's role in the NO/cGMP pathway.