We report the effects of monitored smoking cessation on adrenergic regulation in chronic smokers. The α2 adrenoceptor density of mononuclear leukocytes (MNLs) and plasma catecholamines was analyzed before cessation and 2.3, and 8 weeks after cessation. We found a progressive increase in α-adrenoceptor density after smoking cessatin. During smoking the α-adrenoceptor density after smoking was 1,456 $$ 83 (mean $$ SEM) bindings sites per cell (n = 10), whereas 3 weeks after cessation the the density was 1,774 $$ 157 sites per cell (n = 10: < 0.05), and at 8 weeks, 1,900 $$ 227 sites per cell in (n = 8; p < 0.05), representing an overall increase of 23% Smoking cessation had no effect on binding affinity nor on lymphocyte subgroup distribution. The density of MNL cell β-adrenoceptors in age-matched nonsmoking men was higher, at 1,896 $$ 271 sites per cell, than that of the chronic smokers before cessation, 1,419 $$ 117 sites per cell (n = 14; p < 0.01). Plasma epinephrine decreased as a result of cessation from 0.36 pmol/ml (0.26–0.44m, 95% confidence interval; baseline) to 0.26 pmol/ml (0.20–0.32) at 8 weeks (p <0.05), and norepinephrine decreased from 2.09 pmol/ml (1.38–2.80) to 1.69 pmol/ml (1.14–2.24; p = 0.06). We conclude that stopping smoking progresively increases β2-adrenoceptor density on MNL cells. Eight weeks after cessation the adrenoceptor density reaches the corresponding level of nonsmokers. These reversible changes in adrenergic regulation after smoking cessation may be associated with the relatively rapid reduction in cardiovascular disease risk among ex-smokers.