Cigarette smoking is a major risk factor for the development of atherosclerosis. Smoking might act through endothelial damage. To evaluate microvascular dysfunction, the Transcapillary Escape Rate of Albumin (TERalb), a measure of the unidirectional flux of plasma proteins out of the vascular bed, has been measured in eighteen non-diabetic healthy subjects (14 males, 4 females). No subject had cardiovascular or renal disease, all of them were normotensive (< 140/90 mmHg by ambulatory blood pressure monitoring) and normoalbuminuric (AER range: 2.1-4 μg/min). Seven subjects were current smokers, three were ex-smokers and eight had never smoked. The three groups were similar for age, sBP and dBP, BMI, serum creatinine, total-, LDL- and HDL-cholesterol, Apo-A1, Apo-B and fibrinogen levels. TERalb, calculated from the slope of the linear regression of the log-transformed radioactivity decay of the bolus injected 1 2 5 I human albumin, resulted higher in both current smokers (7.2 ± 1.4%/h, M ± SD) and ex-smokers (7.14 ± 1.5%/h), than in subjects who had never smoked (5.1 ± 1.1%/h, log-transformed TERalb, p = 0.01). Since, serum albumin, haematocrit, plasma volume were similar in all groups, outflux of albumin, calculated as TERalb IVMA (intravascular mass of albumin) was consistently higher in current and ex-smokers than in non-smokers (9.6 ± 2.9 and 8.9 ± 3.7 vs 5.1 ± 1.2 g/h 1.73 m 2 , p = 0.02). Our preliminary results suggest that cigarette smoking is associated with abnormal microvascular function in otherwise asympomatic subjects. Microvascular bed of subjects who have given up smoking, keep memory of the smoke-induced damage.