SYMPATHETIC INNERVATION AND BETA-ADRENOCEPTOR PROFILE OF BLOOD-VESSELS IN THE POSTERIOR REGION OF THE RABBIT KNEE-JOINT

Experiments were performed to investigate the presence and nature of b eta-adrenoceptors in blood vessels supplying the posterior capsule of the rabbit knee joint. Electrical stimulation of the posterior articul ar nerve (PAN) and close intra-arterial injection of adrenaline produc ed vasoconstriction which reversed to vasodilatation with administrati on of the alpha-adrenoceptor antagonist phenoxybenzamine. In almost al l animals close intra-arterial injection of the beta-adrenoceptor agon ist isoprenaline resulted in vasodilatation. Injection of the more sel ective beta-agonists dobutamine, salbutamol and terbutaline also produ ced vasodilatation with a rank potency order of isoprenaline > dobutam ine > salbutamol greater-than-or-equal-to terbutaline. The beta-adreno ceptor antagonist propranolol abolished the dilator responses to adren aline and isoprenaline, and significantly reduced the dilator response s to PAN stimulation in phenoxybenzamine-treated animals. Nerve-mediat ed vasodilatation was also reduced by the substance P antagonist D-Pro 4 D-Trp7,9,10 SP4-11, suggesting that substance P contributes to this dilatation. Dobutamine, a selective beta1-agonist, produced vasodilata tion which was abolished by administration of the selective beta1-anta gonist atenolol. Isoprenaline-induced vasodilatation was substantially reduced by atenolol. The dilator response to isoprenaline appeared to be unaffected by the selective beta2-antagonist ICI118551, but the we ak dilator responses to the selective beta2-agonists salbutamol and te rbutaline were significantly reduced by this antagonist. The results o f this study suggest that beta-adrenoceptors appear to be involved in the sympathetic regulation of rabbit knee joint blood flow, and that t his is predominantly mediated via beta1-adrenoceptors.