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Updated: Aug 29, 2026

Analytical Techniques for Assaying Nitric Oxide Bioactivity
Published on: June 18, 2012
Sildenafil does not improve nitric oxide-mediated endothelium-dependent vascular responses in smokers
Victor Dishy1, Paul A Harris, Rosanna Pierce
1Division of Clinical Pharmacology, General Clinical Research Center, Department of Biomedical Engineering, Vanderbilt University Medical Center, Nashville, TN 37232-6602, USA.
Aims:
To examine the hypothesis that sildenafil, a phosphodiesterase type 5 inhibitor that inhibits cGMP breakdown, could enhance nitric oxide-mediated vasodilation and reverse endothelial dysfunction in chronic smokers.
Methods:
Flow-mediated dilation of the brachial artery and forearm postischemic reactive hyperemia (both nitric oxide-mediated responses) were measured before and after sildenafil 50 mg and placebo in a double-blind, randomized, crossover study in 9 men who were chronic smokers (21 +/- 3 pack years).
Results:
There was no significant change in flow-mediated dilation after either sildenafil (0.18%, 95%CI -1.7-2%) or placebo (0.24%, 95%CI -2.8-3.3%) (P = 0.88 and 0.8, respectively). Sildenafil had no significant effect on resting forearm blood flow or postischemic reactive hyperemia (P = 0.39 and 0.7, respectively). Resting heart rate and blood pressure were unaffected by sildenafil.
Conclusions:
Acute sildenafil administration did not improve endothelial function in chronic smoking men.
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