Sympathetic innervation and beta-adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint.

Abstract

Experiments were performed to investigate the presence and nature of beta-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 alpha-adrenoceptor antagonist phenoxybenzamine. In almost all animals close intra-arterial injection of the beta-adrenoceptor agonist isoprenaline resulted in vasodilatation. Injection of the more selective beta-agonists dobutamine, salbutamol and terbutaline also produced vasodilatation with a rank potency order of isoprenaline > dobutamine > salbutamol > or = terbutaline. The beta-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 SP4-11, suggesting that substance P contributes to this dilatation. Dobutamine, a selective beta 1-agonist, produced vasodilatation which was abolished by administration of the selective beta 1-antagonist atenolol. Isoprenaline-induced vasodilatation was substantially reduced by atenolol. The dilator response to isoprenaline appeared to be unaffected by the selective beta 2-antagonist ICI118551, but the weak dilator responses to the selective beta 2-agonists salbutamol and terbutaline were significantly reduced by this antagonist. The results of this study suggest that beta-adrenoceptors appear to be involved in the sympathetic regulation of rabbit knee joint blood flow, and that this is predominantly mediated via beta 1-adrenoceptors.