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Sympathetic innervation and beta‐adrenoceptor profile of blood vessels in the posterior region of the rabbit knee joint
Author(s) -
Najafipour H,
Ferrell WR
Publication year - 1993
Publication title -
experimental physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0958-0670
DOI - 10.1113/expphysiol.1993.sp003711
Subject(s) - dilator , isoprenaline , atenolol , phenoxybenzamine , medicine , vasodilation , agonist , endocrinology , terbutaline , antagonist , propranolol , chemistry , anesthesia , stimulation , blood pressure , receptor , asthma
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.