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Sildenafil does not improve nitric oxide‐mediated endothelium‐dependent vascular responses in smokers
Author(s) -
Dishy Victor,
Harris Paul A.,
Pierce Rosanna,
Prasad Harish C.,
Sofowora Gbenga,
Bonar Holly L.,
Wood Alastair J. J.,
Stein C. Michael
Publication year - 2004
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1046/j.1365-2125.2003.01974.x
Subject(s) - sildenafil , reactive hyperemia , nitric oxide , medicine , vasodilation , brachial artery , crossover study , anesthesia , forearm , cgmp specific phosphodiesterase type 5 , placebo , endothelium , cardiology , endothelial dysfunction , blood pressure , endocrinology , surgery , alternative medicine , pathology
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.