Effects of cigarette smoking on carotid and radial artery distensibility

OBJECTIVE: Cigarette smoking acutely induces a marked increase of blood pressure and heart rate. This is accompanied by a marked reduction of radial artery distensibility. Whether this reflects an alteration of arterial mechanics of large elastic arteries as well is not established, however. DESIGN AND METHODS: In this study we addressed the acute effects of smoking on the stiffness of a peripheral medium-sized muscular artery and a large elastic vessel. We studied seven healthy normotensive smokers (age 28+/-7 years, mean+/-SEM), in the absence of smoking for at least 24 h. Radial artery (NIUS 02) and carotid artery diameter (WTS) were concomitantly acquired beat-to-beat in the 5 min before, during and after smoking of a cigarette containing 1.2 mg of nicotine. Blood pressure and heart rate were concomitantly recorded by a Finapres device. Radial and carotid artery distensibility were calculated according to the Langewouters and Reneman formulae, respectively. Data were collected for consecutive 30 s periods. Statistical comparisons were performed between the three different phases and, within each phase, between 30 s periods. In five subjects the protocol was repeated after 1 week using a stran rather than a cigarette to obtain data under sham smoking. RESULTS: Smoking increased systolic blood pressure by 14%, diastolic blood pressure by 10% and heart rate by 27%. Radial artery diameter was reduced during smoking (-3.7%) and more so after smoking (-14.8%), while carotid artery diameter did not change significantly either during or after smoking. Radial artery distensibility was also significantly reduced only after smoking (-41.3%, P < 0.01), while carotid artery distensibility was significantly reduced both during (-33.3%) and after smoking (-27.2%) (P < 0.01 versus before). No changes in blood pressure, heart rate and arterial wall mechanics were induced by sham smoking. CONCLUSIONS: Acute cigarette smoking reduces distensibility not only in medium-sized but also in large elastic arteries, therefore causing a systemic artery stiffening. The mechanisms of these effects remain to be determined. However, it is likely that adrenergic mechanisms are responsible for the arterial distensibility alterations.