Sildenafil does not improve nitric oxide-mediated endothelium-dependent vascular responses in smokers.

Dishy V, Harris PA, Pierce R, Prasad HC, Sofowora G, Bonar HL, Wood AJ, Stein CM
Br J Clin Pharmacol. 2004 57 (2): 209-12

PMID: 14748820 · PMCID: PMC1884430 · DOI:10.1046/j.1365-2125.2003.01974.x

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.

MeSH Terms (14)

Adult Brachial Artery Cross-Over Studies Double-Blind Method Endothelium, Vascular Humans Male Nitric Oxide Piperazines Purines Sildenafil Citrate Smoking Sulfones Vasodilator Agents

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