SUMMARYExperiments were performed to investigate the presence and nature of f-adrenoceptors in blood vessels supplying the posterior capsule of the rabbit knee joint. Electrical stimulation of the posterior articular nerve (PAN) and close intra-arterial injection of adrenaline produced vasoconstriction which reversed to vasodilatation with administration of the a-adrenoceptor antagonist phenoxybenzamine. In almost all animals close intra-arterial injection of the /,-adrenoceptor agonist isoprenaline resulted in vasodilatation. Injection of the more selective ,1-agonists dobutamine, salbutamol and terbutaline also produced vasodilatation with a rank potency order of isoprenaline > dobutamine > salbutamol > terbutaline. The /-adrenoceptor antagonist propranolol abolished the dilator responses to adrenaline and isoprenaline, and significantly reduced the dilator responses to PAN stimulation in phenoxybenzamine-treated animals. Nerve-mediated vasodilatation was also reduced by the substance P antagonist D-Pro4 D-Trp7'9'10 SP4 -1, suggesting that substance P contributes to this dilatation. Dobutamine, a selective /31-agonist, produced vasodilatation which was abolished by administration of the selective /ll-antagonist atenolol. Isoprenaline-induced vasodilatation was substantially reduced by atenolol. The dilator response to isoprenaline appeared to be unaffected by the selective I82-antagonist ICI1 18551, but the weak dilator responses to the selective fl2-agonists salbutamol and terbutaline were significantly reduced by this antagonist. The results of this study suggest that /-adrenoceptors appear to be involved in the sympathetic regulation of rabbit knee joint blood flow, and that this is predominantly mediated via fll-adrenoceptors.