Cigarette smoking is a pernicious risk factor for the pathogenesis of coronary artery disease, and endothelial dysfunction is an important antecedent event in this process. This is important, as cigarette smoke is directly toxic to endothelial cells. Inhibitors of angiotensin-converting enzyme (ACE) have been shown to improve endothelial function in diabetes and hypercholesterolaemia, and are a promising option in smokers. We treated 23 subjects (age 38±12 years; mean±S.D.) for 8 weeks with 20 mg of lisinopril in a randomized controlled trial. Endothelial function was assessed by measurement of forearm blood flow responses to intra-arterial infusions of endothelial-dependent and -independent vasodilators and an endothelial-dependent vasoconstrictor [acetylcholine, sodium nitroprusside and monomethyl-l-arginine (l-NMMA) respectively] using venous occlusion plethysmography. Lisinopril significantly increased the forearm blood flow response to acetylcholine by 20% [lisinopril, 3.12±0.37 (mean±S.E.M.); placebo, 2.58±0.25;P = 0.02, 95% confidence intervals (CI) 0.09, 1.06] (values given are ratios of flow in the infused arm to that in the control arm); there was no effect on the response to sodium nitroprusside (lisinopril, 3.97±0.40; placebo, 3.92±0.39; P = 0.84; 95% CI -0.50, 0.61). The vasoconstrictor response to l-NMMA demonstrated a significant improvement (lisinopril, 0.77±0.06; placebo, 0.95±0.05; P < 0.001; 95% CI -0.09, -0.27). In conclusion, these results indicate that ACE inhibition can improve endothelial function in cigarette smokers. We show that lisinopril improves both receptor-mediated and tonic NO release. The mechanism could be either that lisinopril limits the angiotensin II-induced production of superoxide radicals which would normally inactivate NO, or that lisinopril may increase bradykinin-mediated NO release.
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Research Article|
May 24 2001
Lisinopril improves endothelial function in chronic cigarette smokers
Robert BUTLER;
Robert BUTLER
*University Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, U.K.
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Andrew D. MORRIS;
Andrew D. MORRIS
†University Department of Medicine, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, U.K.
‡The Diabetes Centre, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, U.K.
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Allan D. STRUTHERS
Allan D. STRUTHERS
*University Department of Clinical Pharmacology and Therapeutics, Ninewells Hospital and Medical School, Dundee DD1 9SY, Scotland, U.K.
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Publisher: Portland Press Ltd
Received:
March 05 2001
Accepted:
April 03 2001
Online ISSN: 1470-8736
Print ISSN: 0143-5221
The Biochemical Society and the Medical Research Society © 2001
2001
Clin Sci (Lond) (2001) 101 (1): 53–58.
Article history
Received:
March 05 2001
Accepted:
April 03 2001
Citation
Robert BUTLER, Andrew D. MORRIS, Allan D. STRUTHERS; Lisinopril improves endothelial function in chronic cigarette smokers. Clin Sci (Lond) 1 July 2001; 101 (1): 53–58. doi: https://doi.org/10.1042/cs1010053
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