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Analytical Techniques for Assaying Nitric Oxide Bioactivity
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Published on: June 18, 2012

Vascular tolerance to nitroglycerin in ascorbate deficiency.

Gerald Wölkart1, M Verena Wenzl, Matteo Beretta

  • 1Department of Pharmacology and Toxicology, Karl-Franzens-Universität Graz, Universitätsplatz 2, A-8010 Graz, Austria.

Cardiovascular Research
|April 30, 2008
PubMed
Summary
This summary is machine-generated.

Prolonged ascorbate deficiency in guinea pigs led to tolerance to nitroglycerin (GTN)-induced vasodilation. This occurred without impacting nitric oxide (NO)-mediated relaxation, suggesting a specific role for ascorbate in GTN bioactivation.

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Area of Science:

  • Cardiovascular Pharmacology
  • Biochemistry
  • Nutritional Science

Background:

  • Nitroglycerin (GTN) is a vasodilator that releases nitric oxide (NO)-related activators.
  • GTN bioactivation occurs enzymatically via aldehyde dehydrogenase and non-enzymatically with ascorbate.
  • The contribution of endogenous ascorbate to GTN's vasodilatory effects is not fully understood.

Purpose of the Study:

  • To investigate the role of endogenous ascorbate in nitroglycerin (GTN)-induced vasodilation.
  • To determine if ascorbate deficiency impacts GTN's efficacy in a guinea pig model.

Main Methods:

  • Guinea pigs were fed standard or ascorbate-free diets for 2-4 weeks.
  • Aortic ring relaxations and isolated heart responses to GTN and a direct NO donor were measured.
  • GTN metabolism was studied using purified aldehyde dehydrogenase (ALDH2) and isolated mitochondria.

Main Results:

  • Ascorbate deficiency caused scorbutic symptoms and weight loss.
  • GTN-induced vasodilation was significantly impaired in ascorbate-deficient guinea pigs (EC50 increased).
  • Direct NO-mediated vasodilation was minimally affected by ascorbate deficiency.

Conclusions:

  • Prolonged ascorbate deficiency induces tolerance to nitroglycerin.
  • This tolerance develops independently of alterations in the NO/cyclic GMP pathway.
  • Endogenous ascorbate plays a crucial role in nitroglycerin bioactivation and efficacy.