ID 17343 Poster Board 311 Colchicine treatment has known beneficial effects on cardiovascular health and reduces the incidence of cardiovascular disease. Studies in isolated rodent arteries show colchicine enhances β-adrenoceptor-mediated vasodilation. In this translational study, we examined whether this effect of colchicine was present in humans by conducting a double-blinded, placebo controlled intervention study. Middle-aged men with essential hypertension were randomly assigned firstly to acute treatment with either 0.5 mg colchicine or placebo, and subsequently re-randomized for 3 weeks of treatment with either colchicine 0.5 mg twice daily (n=16) or placebo (n=15) followed by a washout period of 48-72 h. The vasodilator responses to isoprenaline, acetylcholine and sodium nitroprusside were determined, as well as arterial pressure, arterial compliance and plasma inflammatory markers. Acute colchicine treatment increased the isoprenaline- and SNP-mediated increase in vascular conductance, but had no effect on the response to acetylcholine. Following the washout period, three weeks of twice daily treatment of colchicine did not induce an accumulated or sustained effect on the β-adrenoceptor response and there was no effect on either arterial pressure, arterial compliance or on the level of measured inflammatory markers. This study provides the first translational evidence for a transient enhancement of β-adrenoceptor-mediated vasodilatation by colchicine in humans. The finding of an acute effect suggests that it may be clinically important to maintain an adequate biovailability of colchicine to support the cardiovascular protective effects that have been observed with colchicine in various clinical trials. This work was supported by a grant from Augustinusfonden (19-3644). TAJ was funded by a Lundbeck Foundation grant (R323-2018-3674). JvH was funded the European Union9s Horizon 2020 research and innovation program under the Marie Sklodowska-Curie scheme (grant agreement no. 081199).