Aging is associated with alterations in-adrenergic receptor (AR) signalling and reduction in cardiovascular responses to AR stimulation. Since exercise can attenuate the age-related impairment in AR signalling and function in myocardium, in this study we tested whether training could exert its favourable effects on vascular AR responses too. We evaluated common carotid arteries responsiveness in isolated vessel rings preparations extracted from 8 aged male Wistar-Kyoto (WKY) rats trained for 6 weeks in a 5 days/week swimming protocol, 10 untrained, age matched and 10 young WKY rats. Vessels were preconstricted with phenylephrine (10^-6M) and vasodilation was assessed in response to the AR agonist isoproterenol (10^-10- 3x10^-8M), the 2AR agonist UK14,304 (10^-9 - 10^-6 M), the muscarinic receptor agonist acetylcholine (10^-9 - 10^-6 M), and to nitroprusside (10^-8 - 10^-5 M). AR density and cytoplasmic -adrenergic receptor kinase 1 (ARK) activity were tested on pooled carotid arteries. ARK expression was assessed in 2 endothelial cell lines from bovine aorta and rat aorta isolated from a 12-week WKY. AR, 2AR and muscarinic responses but not that induced by nitroprusside were depressed in untrained old as compared to young animals. Exercise training restored AR and muscarinic responses while did not affect vasodilation induced by UK 14,304 and nitroprusside. Aged carotid arteries showed reduction in AR number and increased ARK activity. Training counterbalanced these phenomena and restored AR density and ARK activity to levels observed in young rat carotids. Our data indicate that age impairs AR vasorelaxation in rat carotid arteries through AR downregulation and desensitisation. Exercise restores this response and reverts age-related modification in ARs and ARK. Our data support the envision of an important role for ARK in vascular AR vasorelaxation.