Poor ejection fraction in the failing heart is compensated for, in part, by augmented release of circulating catecholamines (Francis et al., 1988). The resulting profile of β-adrenergic receptor (β-AR) desensitisation and down-regulation has been well characterised in cardiac tissue (Bouvier et al., 1989), though the vascular effects remain poorly understood. In this present study, we explored the effects of chronic catecholamine exposure on vascular reactivity in the context of heart failure. Male Wistar rats (200-300g) were treated with the non-selective β-adrenergic agonist, isoprenaline, infused continuously via osmotic mini-pump (Alzet: 4mg/kg/day, subcutaneous administration) for 10 days, leading to cardiac diminished performance. Pumps were implanted under inhalation anaesthesia (isoflurane 3.5% in oxygen) and subsequently, pain relief was administered as required (Temgesic, s.c. administration). Rats were humanely killed by cervical dislocation. Abdominal aorta was freshly-isolated and dissected free of connective tissue, and aortic rings suspended in a myograph and isometric tension estimated in response to agonist challenge (noradrenaline, 1µM). Basal and maximal tension and contractility were quantified with reference to constriction initiated to a high K+ (75mM) depolarisation. All data represent mean ± S.E.M, analysed with student’s t-test and ANOVA as appropriate. Isoprenaline-treated animals showed an increase in the level of basal vascular tension (control, 13.29 ± 0.48mN; treated, 15.98 ± 0.44mN; P<0.05). In both control and treated groups, measures of IC50 demonstrated equal inhibition of noradrenergic contractile responses following α1-AR blockade with prazosin (control, 10-7.9 ± 0.34M; treated, 10-6.8 ± 0.39M; P=0.06), while α2-AR blockade with yohimbine failed to inhibit vasoconstriction in either group. Vasodilatory responses were unaltered by isoprenaline treatment, either for endothelium-dependent (acetylcholine, 1µM) or independent (sodium nitroprusside, 0.1µM) mechanisms, or by stimulation of the downstream signalling cascade in vascular smooth muscle (8-bromo-cyclic-GMP, 100µM). In conclusion, chronic catecholamine exposure does not lead to α-AR desensitisation or endothelial dysfunction in the rat aorta. Despite this, the basal tone of the vessel may be increased; a deficit which could contribute to dysregulated blood flow distribution in heart failure.