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Related Experiment Videos

Nitrates in different vascular beds, nitrate tolerance, and interactions with endothelial function.

E Bassenge1, J Zanzinger

  • 1Institute of Applied Physiology, Freiburg, Germany.

The American Journal of Cardiology
|September 24, 1992
PubMed
Summary

Nitrates, or nitrovasodilators, improve blood flow to the heart by relaxing blood vessels. This action reduces the heart's workload and increases oxygen supply to ischemic areas, mediated by nitric oxide (NO).

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Area of Science:

  • Cardiovascular Pharmacology
  • Physiology

Background:

  • Nitrates are known for their anti-ischemic effects.
  • Their mechanism involves unique vascular relaxation patterns.

Purpose of the Study:

  • To elucidate the detailed mechanism of action of nitrovasodilators in treating myocardial ischemia.
  • To highlight the role of nitric oxide (NO) in mediating these effects.

Main Methods:

  • The study reviews the physiological effects of nitrovasodilators on vascular tone and myocardial oxygen balance.
  • It examines the biochemical pathway involving nitric oxide (NO), soluble guanylyl cyclase, and cyclic guanosine monophosphate (cGMP).

Main Results:

  • Nitrovasodilators decrease cardiac preload and wall tension, reducing myocardial oxygen demand.

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  • They enhance coronary perfusion pressure, improving oxygen delivery to ischemic tissues, particularly the subendocardium.
  • The vasodilatory effect is mediated by nitric oxide (NO)-induced activation of soluble guanylyl cyclase, leading to increased cyclic guanosine monophosphate (cGMP) and suppressed intracellular calcium.

    • Conclusions:

    • Nitric oxide (NO) derived from nitrovasodilators mimics or substitutes for deficient endothelium-derived relaxing factor (EDRF)-mediated vascular control.
    • Therapeutic use of NO-releasing agents addresses impaired endogenous NO production in conditions like ischemia.