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

Abstract:

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.

journal_name

Br J Clin Pharmacol

authors

Dishy V,Harris PA,Pierce R,Prasad HC,Sofowora G,Bonar HL,Wood AJ,Stein CM

doi

10.1046/j.1365-2125.2003.01974.x

keywords:

subject

Has Abstract

pub_date

2004-02-01 00:00:00

pages

209-12

issue

2

eissn

0306-5251

issn

1365-2125

pii

1974

journal_volume

57

pub_type

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