Send to

Choose Destination
Acta Pharmacol Sin. 2005 Apr;26(4):447-52.

Ascorbic acid improves impaired venous and arterial endothelium-dependent dilation in smokers.

Author information

Cardiovascular Pharmacology and Cardiology, Clinical Hospital of Campinas and Faculty of Medical Sciences, State University of Campinas, 13081-970, Campinas, Sao Paulo, Brazil.



To compare the acute effects of ascorbic acid on vasodilation of veins and arteries in vivo.


Twenty-six healthy non-smokers and 23 healthy moderate smokers were recruited in this study. The dorsal hand vein compliance technique and flow-mediated dilation were used. Dose-response curves to bradykinin and sodium nitroprusside were constructed to test the endothelium-dependent and -independent relaxation before and after acute infusion of ascorbic acid.


Smokers had an impaired venodilation with bradykinin compared with non-smokers (68.3%+/-13.2% vs 93.7%+/-20.1%, respectively; P<0.05). Ascorbic acid administration in the dorsal hand vein significantly increased the venodilation with bradykinin in smokers (68.3%+/-13.2% vs 89.5%+/-6.3% before and after infusion, respectively; P<0.05) but not in non-smokers (93.7%+/-20.1% vs 86.4%+/-12.4% before and after infusion, respectively). Similarly, the arterial response in smokers had an impaired endothelium-dependent dilation compared with that in non-smokers (8.8%+/-2.7% vs 15.2%+/-2.3%, respectively; P<0.05) and ascorbic acid restored this response in smokers (8.8%+/-2.7% vs 18.7%+/-6.5% before and after infusion, respectively; P<0.05), but no difference was seen in non-smokers (15.2%+/-2.3% vs 14.0%+/-4.4% before and after infusion, respectively). The endothelium-independent dilation did not differ in both the groups studied. No important hemodynamic change was detected using the Portapress device.


Smokers had impaired endothelium-dependent vasodilation responsiveness in both arterial and venous systems. Ascorbic acid restores this responsiveness in smokers.

[Indexed for MEDLINE]
Free full text

Supplemental Content

Full text links

Icon for Nature Publishing Group
Loading ...
Support Center