It has been shown that inflammation reduces the effectiveness of sympathetic nerves in the regulation of knee joint blood flow, and the joint vascular- ß adrenoceptors are changed due to acute inflammation from a majority of ß-1 to an equality of ß-1 and ß-2 receptors.. To investigate the role of sympathetic nerves in nerve induced vasoconstriction and changes in joint vascular ß-adrenoceptors due to chronic inflammation, in 21 NZW rabbits, chronic inflammation of the knee joint was induced by Antigen induced arthrtis method. In experiment day animals were anesthetized and the caudal femoral artery, a branch of tibial artery, was cannulated to inject the ß -agonists intra-arterially close to the joint. Posterior articular nerve (PAN) was dissected free for electrical stimulation. Electrical stimulation of PAN resulted in 18.1 ± 6.2% reduction of blood flow measured by laser Doppler flowmetry technique. Phentolamine completely blocked the constrictor response and reversed it to vasodilation (+8± 2.2 %).Propranolol (nonselective ß–adrenoceptor antagonist) completely blocked this vasodilation response and reverse it to a vasoconstriction. Atenolol ( ß1 antagonist) nonsignificantly reduced the dilator response but ICI 118551 ( ß2 antagonist ) reduced 50% of this response. Close intra-arterial injection of different doses of ß-agonists, Isoprenaline (nonselective ß agonist ), Dobutamine (ß1 agonist ) and Salbutamol (ß2 agonist) increased the joint blood flow by the potency rank order of “ Isoprenaline > Salbutamole >Dobutamine” .The isoprenaline dose response curve was shifted to the right by ß adrenoceptor antagonists by the potency rank order of propranolol> ICI> atenolol. Overall this study showed that ß2-adrenoceptor response is stronger and suggested that the shift from ß1- to ß2-adrenoceptor subtype started by acute inflammation continued in chronic inflammation and the sympathetic vasoconstrictor response was nearly recovered toward normal compared to acute inflammation.