Background: 

Recent studies have shown that passive smoking impairs vascular endothelial function, but the underlying mechanism has not been totally elucidated. Furthermore, cigarette smoking is known to be associated with an increased plasma homocysteine (Hcy) level.

Aim: 

We investigated if the endothelial dysfunction caused by sidestream cigarette smoke extract (CSE) was due to a nicotine-dependent mechanism. We also decided to compare the effects of cigarette smoke extracts on vasomotor response to those of homocysteine.

Methods: 

CSE was prepared as follows: the cigarette was lit under a Plexiglas box connected to a test tube containing 2ml of phosphate-buffered saline. We studied the endothelial-dependent relaxation in isolated rat aortas incubated for 2 hours with 400ml of CSE in presence or in absence of a-bungarotoxin (1mM), an antagonist of nicotinic acetylcholine (Ach) receptor. We also incubated rat aortas with pure nicotine (0.01, 0.1, and 1mM), DL-Hcy (0.1mM) or L-Hcy (0.1mM).

Results: 

Exposure to 400ml of CSE caused a decrease in the endothelium-dependent relaxations to Ach from 97,81,7% to 78,44,3% (% inhibition of phenylephrine-induced plateau, p < 0,001). Coincubation with a-bungarotoxin showed no significant change compared with CSE. Moreover, concentration-response curves to Ach remained unaltered in preparations incubated with 0.01 and 0.1mM of nicotine. L-Hcy and DL-Hcy had no significant effect on the response to Ach.

Conclusions: 

Our results suggest that the acute endothelial toxicity of passive smoking cannot simply be ascribed to a nicotine-dependent mechanism. We also conclude that, even if cigarette smoke leads to mildly elevated homocysteine levels, it does not show any acute toxicity on vascular endothelial function at those plasma concentrations.