It has been shown that acute inflammation reduces the effectiveness of sympathetic nerves in the regulation of knee joint blood flow. To investigate the role of vascular β- adrenoceptors in this event, 12 NZW rabbits were maintained anaesthetized by 1 % halothane in N₂O/O₂, and acute knee joint inflammation was induced by intra-articular injection of 1 ml of 2% carageenan solution 24 hours before the experiment. On the day of the experiment, a cannula was surgically inserted into the carotid artery to record blood pressure. The medial head of the biceps femoris muscle was removed to provide access to the posterior capsule of the knee and blood flow was measured using a laser flowmeter. Drugs were administered to the joint through a cannula in a branch of the tibial artery. The posterior articular nerve of the knee was also exposed so that it could be electrically stimulated. Electrical stimulation of the posterior articular nerve resulted in a 14.1 ± 3.2% reduction in blood flow measured by laser Doppler flowmetry. This response was reversed to vasodilatation by phentolamine (6.7 ± 1.8%), suggesting the presence of both α and β-adrenoceptors. The vasodilatation response was blocked by propanolol (α β-antagonist) and reduced to about 50% by atenolol (α β₁ -antagonist). Also, close intra-arterial injection of different doses of β-agonists increased the joint blood flow by a potency rank order of isoprenaline (β)>dobutamine (β₁)>salbutamol (β₂). These effects were reduced or blocked by β-antagonists with a potency rank order of propanolol>atenolol. Overall, this study showed a balance between β-adrenoceptor subtypes in the inflamed joint. Compared to our previous investigation on the normal rabbit knee joint in which β₁-adrenoceptors were shown to be predominant, acute inflammation caused a shift of β₁ towards β₂ in the adrenoceptor profile. The clinical significance of this change is not clear at the present time.