Cigarette smoking increases endothelial-derived vasorelaxation in the rat carotid artery in a dose-dependent manner.

While there is clear-cut epidemiologic, morphologic, and functional evidence to suggest that cigarette smoking is deleterious to the cardiovascular system and endothelium, previous experiments with regard to the effect of cigarette smoking on endothelial-derived vasorelaxation are not conclusive. This study examines the effect of cigarette smoking on endothelium-derived vasorelaxation and its relationship to serum nitric oxide concentrations. Fourteen Sprague-Dawley rats (350-500 g) were divided into two groups (N = 7). The experimental group was exposed to six cigarettes (Kentucky 1R4F) per day for 50 days using a Griffith snout exposure method. The two groups were sacrificed and the carotid arteries were mounted on isometric force transducers in a physiologic bath. The arteries were constricted with norepinephrine (1 x 10(-4) M). Vasorelaxation to acetylcholine (Ach) was measured in a dose response manner. Vasorelaxation to nitroglycerin was measured at 10(-4) M. After the rats were sacrificed, blood samples from each rat were examined for total nitrate/nitrite concentration with serum chemiluminescence on a vanadium column. The results were analyzed with ANOVA and the Student's t test. Vasorelaxation to nitroglycerin was 17.42% +/- 0. 44 versus 16.25% +/- 0.42 in the control and smoke exposure groups, respectively (P = 0.19). This experiment counterintuitively demonstrates that cigarette smoking augments endothelial-derived vasorelaxation. No effect was noted in the endothelium-independent vasorelaxation to nitroglycerin. Alternative mechanisms including the presence of hypoxia and exogenous nitric oxide, which lead to endothelial-dependent and -independent vasorelaxation secondary to cigarette smoking, may serve to explain the apparent augmentation of endothelial-derived vasorelaxation. Further experiments with isolated components of smoke will need to be done to resolve the debate.