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Related Experiment Videos

Lisinopril improves endothelial function in chronic cigarette smokers.

R Butler1, A D Morris, A D Struthers

  • 1University Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, U.K. r.butler@btinternet.com

Clinical Science (London, England : 1979)
|June 21, 2001
PubMed
Summary

Angiotensin-converting enzyme (ACE) inhibitors like lisinopril can improve endothelial function in smokers. This study shows ACE inhibition enhances blood vessel responses, potentially by increasing nitric oxide (NO) release.

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Area of Science:

  • Cardiovascular Medicine
  • Pharmacology

Background:

  • Cigarette smoking is a major risk factor for coronary artery disease.
  • Endothelial dysfunction, caused by smoking's toxicity to endothelial cells, is an early event in this disease.
  • Angiotensin-converting enzyme (ACE) inhibitors show promise in improving endothelial function in smokers.

Purpose of the Study:

  • To investigate the effect of ACE inhibition on endothelial function in cigarette smokers.
  • To assess whether lisinopril improves endothelial-dependent and -independent vasodilation and vasoconstriction in smokers.

Main Methods:

  • A randomized controlled trial involving 23 subjects treated with lisinopril or placebo for 8 weeks.
  • Forearm blood flow responses to acetylcholine, sodium nitroprusside, and monomethyl-L-arginine (L-NMMA) were measured using venous occlusion plethysmography.

Related Experiment Videos

  • Endothelial function was assessed by comparing responses to vasodilators and vasoconstrictors between treatment groups.

    • Main Results:

    • Lisinopril significantly increased forearm blood flow response to acetylcholine (endothelial-dependent vasodilator) by 20% (P=0.02).
    • No significant effect of lisinopril was observed on the response to sodium nitroprusside (endothelial-independent vasodilator) (P=0.84).
    • Lisinopril significantly improved the vasoconstrictor response to L-NMMA (P<0.001), indicating enhanced nitric oxide (NO) release.

    Conclusions:

    • ACE inhibition with lisinopril can improve endothelial function in cigarette smokers.
    • Lisinopril enhances both receptor-mediated and tonic nitric oxide (NO) release.
    • Potential mechanisms include limiting angiotensin II-induced superoxide radical production or increasing bradykinin-mediated NO release.