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Circulation. 1996;94:3109-3114

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(Circulation. 1996;94:3109-3114.)
© 1996 American Heart Association, Inc.


Articles

Long-term Smoking Impairs Platelet-Derived Nitric Oxide Release

Kazuya Ichiki, MD; Hisao Ikeda, MD; Nobuya Haramaki, MD; Takafumi Ueno, MD; Tsutomu Imaizumi, MD

the Third Department of Internal Medicine, Kurume University School of Medicine, Kurume, Japan.

Correspondence to Dr Hisao Ikeda, Third Department of Internal Medicine, Kurume University School of Medicine, 67 Asahi-machi, Kurume 830, Japan.

Background Long-term smoking impairs endothelium-dependent vasodilation, which is mediated by nitric oxide (NO). However, it is unknown whether long-term smoking impairs the platelet-derived NO release, which regulates platelet aggregation.

Methods and Results Platelet-derived electrical current induced by collagen was measured with an NO-selective electrode in 12 smokers and 11 nonsmokers. Collagen-induced intraplatelet cGMP and platelet aggregation was measured in smokers and nonsmokers. S-nitroso-N-acetyl-dl-penicillamine, a direct NO donor, dose dependently increased in electrical current (r=.99). Collagen induced platelet aggregation and dose dependently increased electrical current (r=.94). Collagen-induced electrical current and cGMP were significantly augmented by L-arginine, a precursor of NO, and attenuated by NG-monomethyl-L-arginine, an inhibitor of NO synthesis. Significant correlation was found between collagen-induced electrical current and cGMP (r=.73). These findings indicate that the change in electrical current reflects the NO release through the L-arginine–NO pathway in platelets. Collagen-induced electrical current (6.7 versus 13.8 pA; P<.001) and cGMP (1.2 versus 3.0 pmol/109 platelets; P<.005) were significantly lower in smokers than in nonsmokers. Although L-arginine increased cGMP levels in both smokers and nonsmokers, the level was still lower in smokers than in nonsmokers. The inhibitory effect of L-arginine on collagen-induced platelet aggregation was significantly lower in smokers than in nonsmokers (P<.05).

Conclusions These findings provide evidence that platelet-derived NO release is significantly impaired in long-term smokers, resulting in the augmentation of platelet aggregability.


Key Words: smoking • risk factors • platelets • platelet-derived factors • collagen




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